Blue light damage suppressant

Abstract

To provide a blue light disorder inhibitor that shows an excellent blue light disorder inhibiting action.SOLUTION: A blue light disorder inhibitor contains (A) at least one component selected from α-glucosyl rutin, α-glucosyl hesperidin and α-glucosyl naringin and protects constituent cells of skin or eyes or the hair from disorders due to blue light.SELECTED DRAWING: None

Description

Technical Field

[0001] The present invention relates to a blue light damage inhibitor. Background Art

[0002] In recent years, with the advancement of information technology, digital devices such as personal computers and smartphones have rapidly become widespread. LEDs are often used for displays of digital devices. In addition, LED lighting has become increasingly popular due to its low power consumption and long service life. Therefore, in modern life, the human body is exposed to LEDs for long periods of time. LED light contains a large amount of blue light, which is blue light with a wavelength of 400 to 500 nm. Blue light has a short wavelength among visible light and carries high energy, so its effects on the human body have raised concerns. Known effects of blue light on the human body include effects on the eyes such as eye fatigue, eye pain and macular degeneration, effects on the skin such as skin aging, pigmentation and screen dermatitis, as well as systemic effects such as sleep disorders caused by disrupted circadian rhythm, obesity and cancer. As methods for protecting the human body from the effects of blue light, in addition to commercially available eyeglasses with low blue light transmittance, there are known an agent for inhibiting blue light-induced cell growth inhibition containing bilberry extract as an active ingredient (Patent Document 1), and an inhibitor of skin cell proliferation inhibition caused by blue light characterized by containing Goishi tea extract (Patent Document 2), etc. Prior Art Documents Patent Documents

[0003] Patent Document 1 Japanese Unexamined Patent Publication No. 2015-44773 Patent Document 2 Japanese Unexamined Patent Publication No. 2017-178898 Summary of the Invention Problems to be Solved by the Invention

[0004] The object of this invention is to provide a blue light damage inhibitor that exhibits excellent blue light damage suppression effects. [Means for solving the problem]

[0005] The inventors diligently studied to solve the above problems. As a result, they found that the above problems can be solved by having the following configuration, and thus completed the present invention. The present invention relates, for example, to the following [1] to [7]. [1] A blue light damage inhibitor comprising at least one component (A) selected from α-glucosylrutin, α-glucosylhesperidin, and α-glucosylnaringin, which suppresses damage caused by blue light to cells constituting the skin or eyes or to hair. [2] The blue light damage inhibitor according to [1], wherein the damage is the death of cells constituting the skin or eyes. [3] The blue light damage inhibitor according to [1], wherein the damage is damage to the hair cuticle. [4] The blue light damage inhibitor according to [1] or [2], wherein the cells are epidermal keratinocytes or corneal epithelial cells. [5] The blue light damage inhibitor according to any one of [1] to [4], wherein component (A) comprises at least one selected from α-monoglucosylrutin, α-monoglucosylhesperidin, and α-monoglucosylnaringin. [6] A blue light damage inhibitor according to any one of [1] to [5], wherein the content of component (A) is 65% by mass or more. [7] A topical preparation or food / beverage for use on the skin, eyes, or hair that contains a blue light damage inhibitor as described in any of [1] to [6]. [Effects of the Invention]

[0006] According to the present invention, it is possible to provide a blue light damage inhibitor that exhibits excellent blue light damage suppression effects. [Brief explanation of the drawing]

[0007] [Figure 1] Figure 1 is a graph showing the change in the survival rate of normal human epidermal keratinocytes due to blue light irradiation and the effect of α-glucosylrutin (αG-rutin) on that effect. [Figure 2] Figure 2 is a graph showing the change in the survival rate of normal human epidermal keratinocytes due to blue light irradiation and the effect of α-glucosyl hesperidin (αG hesperidin) on that effect. [Figure 3] Figure 3 is a graph showing the changes in the survival rate of normal human epidermal keratinocytes due to blue light irradiation and the effect of α-glucosylnaringin (αGnaringin) on that effect. [Figure 4] Figure 4 is a graph comparing the effects of blue light irradiation on the change in the survival rate of normal human epidermal keratinocytes for α-glucosylrutin (αG-rutin), α-glucosylhesperidin (αG-hesperidin), and α-glucosylnaringin (αG-naringin). [Figure 5] Figure 5 shows the absorption spectrum of α-glucosylrutin (αG-rutin) in the range of 200 nm to 500 nm. [Figure 6] Figure 6 shows the absorption spectrum of α-glucosyl hesperidin (αG hesperidin) in the range of 200 nm to 500 nm. [Figure 7] Figure 7 shows the absorption spectrum of α-glucosylnaringin (αGnaringin) in the range of 200 nm to 500 nm. [Figure 8] Figure 8 shows the spectral distribution of a blue LED. [Modes for carrying out the invention]

[0008] Next, the present invention will be described in detail. <Ingredient (A)> The blue light disorder inhibitor of the present invention comprises at least one component (A) selected from the group consisting of α-glucosyl rutin, α-glucosyl hesperidin and α-glucosyl naringin. Component (A) may comprise any one or any two selected from α-glucosyl rutin, α-glucosyl hesperidin and α-glucosyl naringin, or may comprise all three of α-glucosyl rutin, α-glucosyl hesperidin and α-glucosyl naringin. Among these, those comprising α-glucosyl rutin as component (A) are preferable because the blue light disorder inhibitory effect is high even at a relatively low concentration.

[0009] From the viewpoint of the blue light disorder inhibitory effect, component (A) preferably comprises at least one selected from the group consisting of α-monoglucosyl rutin, α-monoglucosyl hesperidin and α-monoglucosyl naringin.

[0010] The content of component (A) contained in the blue light disorder inhibitor is not particularly limited. For example, examples of the lower limit of the content of component (A) contained in the blue light disorder inhibitor of the present invention include 30% by mass, 40% by mass, 45% by mass, 50% by mass, 60% by mass, 70% by mass, and 80% by mass. Examples of the upper limit of the content of component (A) contained in the blue light disorder inhibitor of the present invention include 100% by mass, 99% by mass, 98% by mass, 95% by mass, 90% by mass, and 85% by mass. As the range of the content of component (A) contained in the blue light disorder inhibitor of the present invention, a range obtained by arbitrarily combining the above lower limit and upper limit can be arbitrarily set, and for example, ranges such as 30 to 100% by mass, 60 to 100% by mass, and 60 to 90% by mass can be set. From the viewpoint of the blue light disorder inhibitory effect, the content of component (A) contained in the blue light disorder inhibitor of the present invention is preferably 65% by mass or more.

[0011] <α-Glucosyl Rutin> α-Glucosyl rutin (also referred to as α-glucosyl rutin) is a general term for compounds in which one or more glucose molecules are added via α1→4 glycosidic linkage to the glucose residue in the rutinose residue of rutin. The α-glucosyl rutin in the present invention may consist of a single type of compound having such a structure, or may be a mixture of two or more types thereof.

[0012] α-Glucosyl rutin can be represented by the following formula (1). In formula (1), n is 0 or an integer of 1 or more, for example, an integer of 1 to 19.

[0013]

Chemical Formula

[0014] α-Glucosyl rutin is a compound contained as a main component in a product known as "enzyme-treated rutin" (sometimes referred to as "glycosyltransferred rutin"). Among α-glucosyl rutin, a compound having only one glucose bound thereto is referred to as "α-monoglucosyl rutin", and a compound having two or more glucose molecules bound thereto is referred to as "α-polyglucosyl rutin". That is, in formula (1), α-monoglucosyl rutin is a compound where n is 0, and α-polyglucosyl rutin is generally a compound where n is 1 to 19.

[0015] Enzyme-treated rutin is an aggregate of compounds produced by enzymatic treatment on the sugar moiety of rutin, and usually comprises a mixture of compounds differing in the number of glucose molecules bound to rutin, for example, a mixture composed of α-monoglucosyl rutin and α-polyglucosyl rutin. In addition, since enzyme-treated rutin is generally produced by enzymatic treatment, it may also contain unreacted rutin and other derivatives, for example, isoquercitrin. Note that isoquercitrin (sometimes also referred to as isoquercitrin) is a compound in which β-D-glucose is bound to the 3-hydroxyl group of the quercetin skeleton, in other words, a compound in which the rhamnose residue in the rutinose residue of rutin is cleaved.

[0016] Enzyme-treated rutin is a product obtained, for example, by treating rutin with a glycosyltransferase (such as cyclodextrin glucanotransferase (CGTase, EC2.4.1.19), an enzyme that has the function of adding glucose to rutin) in the presence of α-glucosyl sugar compounds (such as cyclodextrin or partially hydrolyzed starch) (referred to as "first enzyme-treated rutin" in this specification).

[0017] The first enzyme-treated rutin is a composition containing aggregates of various α-glucosylrutins with different numbers of bound glucose molecules, namely α-monoglucosylrutin and α-polyglucosylrutin, and unreacted rutin. If necessary, the first enzyme-treated rutin can be purified using, for example, a porous synthetic adsorbent and an appropriate eluate to remove sugar donors and other impurities, further reduce the rutin content, and increase the purity of α-glucosylrutin to obtain the first enzyme-treated rutin (purified α-glucosylrutin).

[0018] Furthermore, by treating the first enzyme-treated rutin with an enzyme having glucoamylase activity that cleaves α-1,4-glucosidic bonds at the glucose level, such as glucoamylase (EC3.2.1.3), in α-glucosylrutin to which multiple glucose molecules are attached, all glucose residues except for one glucose residue directly attached to the glucose residue (in the rutinose residue) of the rutin itself are cleaved, thereby obtaining enzyme-treated rutin containing a large amount of α-monoglucosylrutin (referred to herein as "second enzyme-treated rutin"). This enzyme treatment does not cause the glucose residue in the rutinose residue directly bound to the quercetin skeleton to be cleaved from the quercetin skeleton.

[0019] In the blue light damage suppressant of the present invention, considering the effects of the present invention, it is preferable to use an enzyme-treated rutin composition containing α-glucosylrutin, and either a composition containing first enzyme-treated rutin or second enzyme-treated rutin may be used.

[0020] Considering the effects of the present invention, the enzyme-treated rutin is preferably a mixture containing at least α-glucosylrutin and further containing isoquercitrin. Such a mixture can be produced by the following procedure: (i) preparing the first enzyme-treated rutin described above; (ii) treating the first enzyme-treated rutin with an enzyme having glucoamylase activity to convert almost all of the α-glucosylrutin to α-monoglucosylrutin; and (iii) simultaneously treating it with an enzyme having rhamnosidase activity to convert almost all of the unreacted rutin to isoquercitrin.

[0021] Commercially available enzyme-treated rutin products include, for example, "αG Rutin PS-C," "αG Rutin PS," "αG Rutin P," and "αG Rutin H" from Toyo Sugar Refining Co., Ltd. "αG Rutin PS-C" is a composition containing 65% by mass of α-monoglucosylrutin and 15% by mass of isoquercitrin. "αG Rutin PS" is a composition containing 65% by mass of α-monoglucosylrutin and 15% by mass of isoquercitrin. "αG Rutin P" is a composition containing 60% by mass of α-glucosylrutin, 10% by mass of rutin, and 1% isoquercitrin.

[0022] α-monoglucosylrutin is preferred as the α-glucosylrutin. This is because the molecular weight of α-monoglucosylrutin is smaller than that of α-polyglucosylrutin, resulting in a higher number of molecules per unit mass for α-monoglucosylrutin, which is considered advantageous in terms of its effects.

[0023] The presence of various α-glucosylrutins and other components in enzyme-treated rutin can be confirmed by HPLC chromatogram, and the content of each component, or the purity of a specific desired component, can be calculated from the peak area of ​​the chromatogram.

[0024] The method for producing α-glucosylrutin is not particularly limited, and known methods can be used. As mentioned above, it is preferable to produce it by enzymatic treatment of rutin because it yields a good yield and is easy to manufacture. The method for obtaining and preparing rutin is not particularly limited, and compounds that are generally manufactured and sold as reagents or purified products may be used, or compounds prepared by extraction from raw materials such as the peels of citrus fruits (mandarins, oranges, etc.) or buckwheat seeds may be used.

[0025] <α-Glucosyl Hesperidin> α-glucosyl hesperidin (also called α-glucosyl hesperidin) is a general term for compounds in which one or more glucose molecules are attached to the hydroxyl group in the rutinose unit of hesperidin via an α-1,4 linkage. In this invention, α-glucosyl hesperidin may consist of one compound having such a structure alone, or it may be a mixture of two or more such compounds. Hesperidin is a compound in which β-rutinose (6-O-α-L-rhamnosyl-β-D-glucose) is attached to the hydroxyl group at position 7 of hesperetin, i.e., a hesperetin glycoside.

[0026] α-Glucosyl hesperidin can be represented by the following formula (2). In formula (2), n is an integer greater than or equal to 0 or 1, for example, an integer from 1 to 19.

[0027] [ka] ...(2)

[0028] α-glucosyl hesperidin is a compound that is the main component of materials known as "enzyme-treated hesperidin" (sometimes called "glycosylated hesperidin"). Among α-glucosyl hesperidins, those with only one glucose molecule attached are called "α-monoglucosyl hesperidin," and those with two or more glucose molecules attached are called "α-polyglucosyl hesperidin." In other words, in equation (2), α-monoglucosyl hesperidin is a compound where n is 0, and α-polyglucosyl hesperidin is generally a compound where n is between 1 and 19.

[0029] Enzyme-treated hesperidin is an aggregate of compounds produced by enzymatic treatment of hesperidin with respect to its sugars, and typically includes a mixture of compounds with different numbers of glucose molecules bound to hesperidin, such as a mixture of α-monoglucosylhesperidin and α-polyglucosylhesperidin. Enzyme-treated hesperidin may also contain not only α-glucosylhesperidin but also unreacted hesperidin and hesperidin derivatives other than α-glucosylhesperidin, such as 7-glucosylhesperetin (also called other hesperidin derivatives). However, it is preferable that enzyme-treated hesperidin does not contain hesperetin.

[0030] Examples of the enzymatic treatment of hesperidin with respect to sugars are as follows: (1) Hesperidin is treated with a glycosyltransferase in the presence of a sugar donor, and glucose is added to the glucose unit of hesperidin via an α-1,4 linkage, thereby producing α-glucosylhesperidin, and a composition containing unreacted hesperidin and α-glucosylhesperidin is obtained (first enzymatic treatment hesperidin). (2) The α-glucosylhesperidin produced in (1) is treated with glucoamylase or the like, and all but one molecule of glucose is cleaved from the glucose chain attached to the glucose unit of hesperidin, thereby producing α-monoglucosylhesperidin, and a composition containing unreacted hesperidin and α-monoglucosylhesperidin is obtained (second enzymatic treatment hesperidin). (3) The unreacted hesperidin from (2) above is treated with α-L-rhamnosidase to cleave the rhamnose contained in the rutinose unit of hesperidin, thereby generating 7-glucosylhesperetin, and a composition containing 7-glucosylhesperetin and α-monoglucosylhesperidin is obtained (third enzyme-treated hesperidin).

[0031] An example of the first enzymatic treatment is the application of a glycosyltransferase (e.g., cyclodextrin, partially hydrolyzed starch, etc., an enzyme that has the function of adding glucose to hesperidin) to hesperidin in the presence of an α-glucosyl sugar compound (e.g., cyclodextrin, partially hydrolyzed starch).

[0032] In the blue light damage inhibitor of the present invention, considering the effects of the present invention, it is preferable to use enzyme-treated hesperidin, which is a composition containing α-glucosyl hesperidin, and any of the compositions of first enzyme-treated hesperidin, second enzyme-treated hesperidin, and third enzyme-treated hesperidin may be used.

[0033] Considering the effects of the present invention, the enzyme-treated hesperidin is preferably a mixture containing at least α-glucosyl hesperidin, and further containing either hesperidin or 7-glucosyl hesperetin, or both.

[0034] Examples of commercially available enzyme-treated hesperidin include "αG Hesperidin PS-CC" and "αG Hesperidin PA-T" from Toyo Sugar Refining Co., Ltd. "αG Hesperidin PS-CC" contains 80% by mass or more of α-monoglucosyl hesperidin and also contains 7-glucosyl hesperetin. "αG Hesperidin PA-T" contains 75% by mass or more of α-monoglucosyl hesperidin and also contains hesperidin.

[0035] α-monoglucosylhesperidin is preferred as the α-glucosylhesperidin. This is because the molecular weight of α-monoglucosylhesperidin is smaller than that of α-polyglucosylhesperidin, resulting in a higher number of molecules per unit mass for α-monoglucosylhesperidin, which is considered advantageous in terms of efficacy.

[0036] α-Monoglucosylhesperidin can be produced by treating α-polyglucosylhesperidin with a sugar hydrolase, cleaving all glucose molecules bound to hesperidin while leaving only one molecule (second enzyme-treated hesperidin). Examples of sugar hydrolases include enzymes with glucoamylase activity that cleave α-1,4-glucosidic bonds at the glucose level, such as glucoamylase (EC3.2.1.3). The proportion of α-monoglucosylhesperidin in α-glucosylhesperidin can be adjusted by controlling the temperature or time conditions of the enzyme treatment with glucoamylase, and methods for purifying and separating α-monoglucosylhesperidin from a mixture of enzyme-treated hesperidins are also known.

[0037] The presence of various α-glucosyl hesperidins, hesperidins, and other components in enzyme-treated hesperidin can be confirmed by HPLC chromatogram, and the content of each component, or the purity of a specific desired component, can be calculated from the peak area of ​​the chromatogram.

[0038] The method for producing α-glucosyl hesperidin is not particularly limited, and known methods can be used. It is preferable to produce it by enzymatic treatment of hesperidin, as this yields a good yield and is easy to manufacture. The method for obtaining and preparing hesperidin is not particularly limited, and compounds that are generally manufactured and sold as reagents or purified products may be used, or compounds prepared by extraction from raw materials such as the peels of citrus fruits (mandarins, oranges, etc.) may be used.

[0039] <α-glucosylnaringin> α-glucosylnaringin (also called α-glucosylnaringin) is a general term for compounds in which one or more molecules of glucose are attached to the hydroxyl group of naringin. Naringin is a type of flavonoid having a structure in which neohesperidose (L-rhamnosyl-(α1→2)-D-glucose) is β-bonded to the hydroxyl group at position 7 of the naringenin (5,7,4'-trihydroxyflavanone) skeleton. α-glucosylnaringin has a structure in which one or more molecules of α-glucose are attached to at least one of the hydroxyl groups of the glucose residue at position 3 (3'') in the neohesperidose residue and the hydroxyl group at position 4 (4') of the phenyl group in the naringenin skeleton. In the present invention, α-glucosylnaringin may consist of one type of compound having such a structure alone, or it may be a mixture of two or more types.

[0040] α-glucosylnaringin can be represented by the following formula (3). In formula (3), R 1 m and R 2In this equation, n represents the number of α-glucose residues attached to the 3'' and 4' positions, respectively, and is an independent integer between 0 and 25, usually between 0 and 25. However, for equation (3) to represent "α-glucosylnaringine", it must satisfy m+n≧1, meaning that at least one α-glucose molecule is attached to naringine (when m=n=0, i.e., R 1 , R 2 If both are -H, then equation (3) represents "naringin".

[0041] [ka] ...(3)

[0042] α-glucosylnaringin is a compound that is the main component of materials known as "enzyme-treated naringin" (sometimes called "glycosylated naringin"). Among α-glucosylnaringins, those with only one glucose molecule attached are called "α-monoglucosylnaringin," and those with two or more glucose molecules attached are called "α-polyglucosylnaringin."

[0043] Enzyme-treated naringin is, for example, a product obtained by reacting a mixture of naringin and a sugar donor (e.g., dextrin) with a glycosyltransferase (e.g., cyclodextrin glucosyltransferase) (hereinafter referred to as "first enzyme-treated naringin"), and is an aggregate of various compounds in which one or more glucose molecules are attached to the hydroxyl group of naringin. Therefore, enzyme-treated naringin usually includes a mixture of compounds with different numbers of glucose molecules attached to naringin, for example, a mixture consisting of α-monoglucosylnaringin and α-polyglucosylnaringin. In addition to α-glucosylnaringin, it may also include unreacted naringin or naringin derivatives other than α-glucosylnaringin (also called other naringin derivatives), such as 7-glucosylnaringenin.

[0044] For example, the basic method for producing the first enzyme-treated naringin can be found in Japanese Patent Publication No. 4-13691. If necessary, the first enzyme-treated naringin can be purified using, for example, a porous synthetic adsorbent and an appropriate eluate to remove sugar donors and other impurities, further reduce the naringin content, and obtain the first enzyme-treated naringin (purified α-glucosylnaringin) with increased purity.

[0045] As α-glucosylnaringin, at least one α-glucosylnaringin selected from 3''-α-monoglucosylnaringin (in formula (3), m=1, n=0), 4'-α-monoglucosylnaringin (likewise m=0, n=1), and 3''-4'-α-diglucosylnaringin (likewise m=1, n=1) is preferred, with 3''-α-monoglucosylnaringin being more preferred. This is because the molecular weight of α-monoglucosylnaringin is smaller than that of α-polyglucosylnaringin, resulting in a higher number of molecules per unit mass for α-monoglucosylnaringin, which is considered advantageous in terms of efficacy.

[0046] Enzyme-treated naringin containing a large amount of the three types of α-mono / diglucosylnaringin described above (referred to as "second enzyme-treated naringin" in this specification) can be obtained, for example, by treating the first enzyme-treated naringin described above with an enzyme having glucoamylase activity, and cleaving the sugar chain in which two or more α-glucose molecules are linked by α-1,4 bonds, which has been transferred to the 3'' and / or 4' positions of naringin by the glycosyltransferase, leaving only the α-glucose residue equivalent to one molecule at the base. Furthermore, by treating the second enzyme-treated naringin with an enzyme having α-glucosidase activity, and cleaving the α-glucose residue equivalent to one molecule directly bound to the hydroxyl group at the 4' position, it is possible to obtain enzyme-treated naringin that retains 3''-α-monoglucosylnaringin and contains little to no 4'-α-monoglucosylnaringin and 3''-4'-α-diglucosylnaringin (referred to as "third enzyme-treated naringin" in this specification). For basic methods of producing the second and third enzyme-treated naringin, see, for example, Japanese Patent Publication No. 2002-199896.

[0047] Furthermore, by reacting the third enzyme-treated naringin with α-L-rhamnosidase, rhamnose contained in the rutinose unit of naringin is cleaved, thereby generating 7-glucosylnaringenin, and an enzyme-treated naringin containing 7-glucosylnaringenin and α-monoglucosylnaringin (referred to as "fourth enzyme-treated naringin" in this specification) is obtained.

[0048] Furthermore, if the first enzyme-treated naringin is treated with transglucosidase, since transglucosidase is an enzyme that possesses both glucoamylase and α-glucosidase activity, a third enzyme-treated naringin rich in 3''-α-monoglucosylnaringin can be obtained in a single step instead of the two-step process described above. In addition, if necessary, an enzyme with β-glucosidase activity may be treated with the third enzyme-treated naringin (or simultaneously with transglucosidase on the first enzyme-treated naringin) to cleave the neohesperidose residue (which has not been modified by glycosyltransferase) present in the unreacted naringin dissolved in the aqueous solution from its aglycone, naringenin. Since the naringenin produced by such treatment has lower solubility than naringin, it can be easily removed from the aqueous solution as a precipitate, making it possible to recover 3''-α-monoglucosylnaringin from the aqueous solution in higher purity.

[0049] In the blue light damage inhibitor of the present invention, considering the effects of the present invention, it is preferable to use an enzyme-treated naringin composition containing α-glucosylnaringin, and any of the first enzyme-treated naringin, second enzyme-treated naringin, third enzyme-treated naringin, and fourth enzyme-treated naringin compositions may be used.

[0050] Considering the effects of the present invention, the enzyme-treated naringin is preferably a mixture containing at least α-glucosylnaringin, and further containing either or both of naringin and 7-glucosylnaringenin.

[0051] The presence of various α-glucosylnaringins, naringins, and other components in enzyme-treated naringin can be confirmed by HPLC chromatogram, and the content of each component, or the purity of a specific desired component, can be calculated from the peak area of ​​the chromatogram.

[0052] The method for producing α-glucosylnaringin is not particularly limited, and known methods can be used. It is preferable to produce it by enzymatic treatment of naringin, as this yields a good yield and is easy to manufacture. The method for obtaining and preparing naringin is not particularly limited, and compounds that are generally manufactured and sold as reagents or purified products may be used, or compounds prepared by extraction from raw materials such as the peels of citrus fruits (such as summer oranges and grapefruits) may be used.

[0053] <Cells that make up the skin> In this invention, "skin" refers to the skin of the entire body, including accessory organs (sweat glands, sebaceous glands, apocrine glands, eccrine glands, hair follicles, and nails) and lips (skin portion, transitional portion, and mucous membrane portion). The location of the skin is not particularly limited, but because it is easily exposed to blue light, the skin is preferably the skin of the face, head, neck, hands, or arms, and more preferably the skin of the face or head (scalp).

[0054] The cells that make up the skin can be any cells that make up the skin, and are not particularly limited. Examples of cells that make up the skin include epidermal keratinocytes of the epidermis, fibroblasts of the dermis, adipocytes of the subcutaneous fat layer, and other cells such as epidermal Langerhans cells, dermal dendritic cells, melanocytes, Merkel cells, histiocytes, mast cells, plasma cells, and stem cells, and may also include cells that make up accessory organs, such as sebaceous glands, sweat glands, and hair follicles. Because the skin is susceptible to damage from blue light, the cells that make up the skin are preferably epidermal keratinocytes, dermal fibroblasts, or melanocytes, with epidermal keratinocytes being more preferred.

[0055] The origin of the cells that make up the skin is not particularly limited, but primate mammals including mice, rats, hamsters, guinea pigs, dogs, pigs, monkeys, or humans are preferred, and humans are more preferred.

[0056] <Cells that make up the eye> The term "eye" refers to the eyeball, optic nerve, and its appendages (eyelids, lacrimal gland). The cells that make up the eye can be any cells that make up the eye, and are not particularly limited, but are preferably cells that make up the eyeball.

[0057] Examples of cells that make up the eyeball include cone cells, rod cells, bipolar cells, horizontal cells, amacrine cells, melanopsin ganglion cells, and retinal pigment epithelial cells present in the retina; corneal epithelial cells, corneal stromal cells (corneal keratocytes, corneal fibroblasts), and corneal endothelial cells present in the cornea; iris cells and iris pigment epithelial cells present in the iris; lens fiber cells and lens epithelial cells present in the lens; ciliary body achromatoe epithelial cells and pigment epithelial cells present in the ciliary body; and ocular choroidal fibroblasts present in the choroid. Because the eye is susceptible to damage from blue light, the cells that make up the eyeball are preferably corneal epithelial cells, cone cells, or rod cells, with corneal epithelial cells being more preferred.

[0058] The origin of the cells that make up the eye is not particularly limited, but primate mammals including mice, rats, hamsters, guinea pigs, dogs, pigs, monkeys, or humans are preferred, and humans are more preferred.

[0059] <Hair> Hair is not particularly limited and may include, for example, scalp hair, eyebrows, eyelashes, beard, and body hair, but scalp hair is preferred. The origin of the hair is not particularly limited, but it is preferably from primate mammals including mice, rats, hamsters, guinea pigs, dogs, pigs, monkeys, or humans, with humans being more preferred. The hair may be virgin hair, or it may be hair that has been previously treated with hair colorants, bleaches, permanent wave agents, straightening agents, or treatment agents.

[0060] <Blue light damage suppressant> The blue light damage inhibitor of the present invention suppresses damage caused by blue light to cells constituting the skin or eyes, or to hair. In this invention, blue light refers to light with a wavelength of 400 to 500 nm. In this invention, blue light-induced injury means a condition in which some or all of the normal function or structure of cells constituting the skin or eyes, or of hair, is impaired due to exposure to blue light.

[0061] Damage caused by blue light to cells constituting the skin or eyes may include, for example, inhibition or cessation of the respiration, metabolism, DNA replication, transcription, or translation of the cells, damage, destruction, or oxidation of cell structure or cellular components, inhibition or cessation of the cell cycle, or intracellular signaling, or more specifically, changes in cell morphology, inhibition or cessation of proliferation or differentiation, cellular senescence, cell death (necrosis, apoptosis), DNA damage, mutation, inflammation, excessive pigment production, severance or reduction of elastic fibers, etc. Since evaluation can be easily performed, damage caused by blue light to cells constituting the skin or eyes is preferably changes in morphology, inhibition or cessation of proliferation or differentiation, or cell death, and more preferably cell death.

[0062] The method for evaluating the effect of suppressing damage caused by blue light to cells constituting the skin or eyes is not particularly limited, and known methods can be used. For example, if the degree of damage to cells exposed to blue light with the test substance added is lower than the degree of damage to cells exposed to blue light without the test substance added, the test substance can be evaluated as having an effect of suppressing damage caused by blue light. If the damage caused by blue light is cell death, then, for example, as described later in the examples, if the survival rate of cells exposed to blue light with the test substance added is higher than the survival rate of cells exposed to blue light without the test substance added, when the survival rate of cells not exposed to blue light is set to 100%, then the test substance can be evaluated as having an effect of suppressing damage caused by blue light. In this case, the cell survival rate is preferably 40% or more, more preferably 50% or more, even more preferably 60% or more, and particularly preferably 70% or more.

[0063] Damage to hair caused by blue light may be damage to the cuticle, cortex, or medulla, and examples include changes in the surface condition or feel of the hair, such as split ends, breakage, dryness, and loss of shine; changes in physical properties such as tensile strength; changes in the microstructure of the hair cuticle, cortex, or medulla; and oxidation or changes in the functional groups of proteins that make up the hair. Because it can be easily evaluated, damage to hair caused by blue light is preferably damage to the cuticle, and more preferably changes in the microstructure of the cuticle.

[0064] There are no particular restrictions on the method for evaluating the effect of the test substance on suppressing damage to hair caused by blue light, and known methods can be used. For example, if the degree of damage to hair exposed to blue light with the test substance added is lower than the degree of damage to hair exposed to blue light without the test substance added, then the test substance can be evaluated as having an effect on suppressing damage caused by blue light.

[0065] In this invention, "suppression of blue light damage" encompasses the prevention, improvement, reduction, elimination, and alleviation of symptoms of the above-mentioned blue light damage, as well as treatment, healing, and promotion of healing.

[0066] The mechanism of action of the blue light damage inhibitor of the present invention is unknown, but since component (A) does not absorb blue light, it is presumed that the action is due to the physiological effects of component (A).

[0067] The blue light damage inhibitor may contain at least one component (A) selected from α-glucosylrutin, α-glucosylhesperidin, and α-glucosylnaringin, and may consist only of component (A), or may further contain known optional components such as excipients, stabilizers, wetting agents, and emulsifiers, as long as they do not interfere with the blue light damage inhibitory effect of component (A). Furthermore, the blue light damage inhibitor may be a composition containing component (A), at least one selected from enzyme-treated rutin, enzyme-treated hesperidin, and enzyme-treated naringin, or it may contain at least one selected from enzyme-treated rutin, enzyme-treated hesperidin, and enzyme-treated naringin.

[0068] Examples of blue light damage inhibitors containing the aforementioned component (A) include commercially available products such as "αG Rutin PS," "αG Rutin P," "αG Rutin H," "αG Hesperidin PS-CC," and "αG Hesperidin PA-T" from Toyo Sugar Refining Co., Ltd. These products themselves may be used as blue light damage inhibitors, or compositions containing these products may be used as blue light damage inhibitors.

[0069] <Uses of blue light damage suppressants> The uses of the blue light damage inhibitor are not particularly limited, but since the blue light damage inhibitor of the present invention has a high effect in suppressing damage caused by blue light, it can be administered to the body once or multiple times for the purpose of preventing or improving blue light damage that occurs in cells constituting the skin or eyes or in hair in living organisms.

[0070] Blue light damage inhibitors are useful in preventing or improving diseases and symptoms involving blue light damage to cells that make up the skin or eyes. For example, they contribute to preventing or improving the onset and progression of skin aging, pigmentation, screen dermatitis, eye strain or pain, and macular degeneration.

[0071] The dosage of the blue light damage inhibitor can be appropriately selected depending on the type or severity of blue light damage or the disease or symptoms associated with blue light damage. For example, when the blue light damage inhibitor is administered orally, a daily dose of 10 mg to 700 mg of component (A) is preferred, and 100 mg to 500 mg is more preferred, from the viewpoint of blue light damage inhibitory effect. When the blue light damage inhibitor is applied topically, an appropriate amount of a composition containing component (A) at a concentration of preferably 0.01 to 2% by mass, more preferably 0.025 to 0.5% by mass, can be administered, from the viewpoint of blue light damage inhibitory effect. Furthermore, the daily dose can be divided into, for example, 1 to 3 doses per day, and it is preferable to administer it in 2 or 3 doses.

[0072] The duration of administration of blue light damage inhibitors should be appropriately selected depending on the type or severity of blue light damage or the disease or symptoms associated with blue light damage. From the viewpoint of blue light damage suppression effectiveness, it is preferably 7 to 80 days, more preferably 14 to 60 days.

[0073] <Formulations containing blue light damage inhibitors> The blue light damage inhibitor may be administered directly to the body, or it may be administered as a formulation containing an effective amount of the blue light damage inhibitor together with a pharmaceutically acceptable carrier. The formulations containing the blue light damage inhibitor are not particularly limited and include, for example, topical preparations, injectable preparations, or food and beverages, but are preferably topical preparations or food and beverages, and more preferably topical preparations. The method of administration of the formulation containing the blue light damage inhibitor is not particularly limited and can be administered orally or parenterally. The formulation is preferably administered parenterally, more preferably topically, and even more preferably topically to the skin, hair, or eyes, as it is easy to administer.

[0074] Formulations containing blue light damage inhibitors can be manufactured by adding the blue light damage inhibitor in accordance with methods commonly used for such formulations. The blue light damage inhibitor may be added at the beginning of the manufacturing process, or at the middle or end of the manufacturing process, and the method of addition may be selected appropriately from mixing, kneading, dissolving, immersion, spraying, misting, coating, etc., depending on the form of the formulation.

[0075] Since component (A), which is the active ingredient of the blue light damage inhibitor, has good water solubility, it can be uniformly dissolved or dispersed even when added to water or formulations with a high water content.

[0076] <Topical preparations> In this invention, "topical preparation" refers to a preparation applied directly to the surface of the skin, eyes, hair, etc., and may be a pharmaceutical product, a quasi-drug, or a cosmetic product. External preparations are not limited in terms of properties or dosage form, as long as they can be applied to or penetrate the body surface, such as the skin, mucous membranes, eyes, nails, or hair, and can be in the form of a liquid, emulsion, cream, gel, mousse, spray, or a two-part preparation by mixing these.

[0077] One aspect of the present invention is a topical preparation for use on the skin, eyes, or hair, comprising the blue light damage inhibitor, and preferably a topical preparation for use on the skin, eyes, or hair, comprising the blue light damage inhibitor.

[0078] Examples of topical preparations for use on the skin include: skincare cosmetics such as lotions, emulsions, skin creams, face creams, eye creams, serums, and masks; makeup cosmetics such as foundations and eyeshadows; cleansing agents such as facial cleansers; body care cosmetics such as bath additives and body creams; topical skin preparations such as ointments, liniments, and lotions; topical preparations for use on the scalp such as hair growth agents, hair tonics, serums, and oils; topical preparations for use on the lips such as lip balms, lipsticks, and lip glosses; and topical preparations for use on the nails such as nail polish, base coats, top coats, and nail serums. Topical preparations used on the skin are preferably skincare cosmetics or topical skin preparations, and more preferably skin creams, face creams, eye creams, or serums.

[0079] The topical preparation for use on the skin preferably contains component (A) at a concentration of 0.01 to 2% by mass, more preferably 0.025 to 0.5% by mass, from the viewpoint of suppressing blue light damage. The topical preparation for use on the skin is preferably used at a dose of 0.1 to 5 g, more preferably 0.5 to 2 g per day.

[0080] For topical preparations applied to the skin, ingredients commonly used in cosmetics, pharmaceuticals, and other topical skin preparations and cleansers may be appropriately blended as needed, within limits that do not impair the effects of the present invention. These ingredients include, for example, oils and fats, waxes, hydrocarbon oils, ester oils, higher alcohols, silicone oils, UV absorbers, UV scattering agents, moisturizers, surfactants, water-soluble polymers, thickeners, powders, skin protectants, whitening agents, wrinkle-improving agents, anti-aging agents, plant extracts, preservatives, anti-inflammatory agents, pH adjusters, metal ion chelating agents, antioxidants, stabilizers, fragrances, dyes, pigments, etc. These ingredients may be used individually or in combination of two or more.

[0081] Because it is easy to apply and provides a more sufficient blue light damage suppression effect, it is preferable to include a moisturizer in topical preparations used on the skin. Examples of humectants include: viscosity modifiers such as cellulose-based polymer compounds, vinyl-based polymer compounds and their salts; polysaccharides such as xanthan gum, dextrin, dextran, and heparin; mucopolysaccharides such as hyaluronic acid, sodium hyaluronate, and sodium chondroitin sulfate; polyhydric alcohols such as propylene glycol, 1,3-butylene glycol, polyethylene glycol, and glycerin; sugars such as glucose, trehalose, lactose, and sorbitol; and sugar derivatives of polyhydric alcohols such as glyceryl glucoside. For moisturizers incorporated into topical preparations for use on the skin, polyhydric alcohols or sugar derivatives of polyhydric alcohols are preferred, glycerin, 1,3-butylene glycol, or glyceryl glucoside are more preferred, and glyceryl glucoside is even more preferred. The amount of moisturizer contained in topical preparations for use on the skin is not particularly limited, but from the viewpoint of the stability of the topical preparation and its moisturizing effect, it is preferably 0.5 to 20% by mass, more preferably 2 to 15% by mass, and even more preferably 2 to 10% by mass.

[0082] There are no particular restrictions on the method for manufacturing topical preparations for use on the skin, and they can be manufactured using well-known methods. For example, they can be manufactured by mixing and stirring raw materials using common equipment such as homogenizers, dispersers, dispa mixers, propeller mixers, turbine mixers, and colloid mills.

[0083] Examples of topical preparations for use on the eyes include eye ointments, eye gels, eye creams, and eye drops. Eye drops are preferred as topical preparations for use on the eyes because they are easy to administer.

[0084] The topical preparation for use on the eyes preferably contains component (A) at a concentration of 0.01 to 2% by mass, more preferably 0.025 to 0.5% by mass, from the viewpoint of suppressing blue light damage. The topical preparation for use on the eyes is preferably used at a dose of 0.01 to 0.5 g, more preferably 0.05 to 0.3 g per day.

[0085] Topical preparations for use on the eyes may contain, as necessary and within limits that do not impede the effects of the present invention, various components (including pharmacologically active and physiologically active components) commonly used in ophthalmic topical preparations. The types of such components are not particularly limited and include, for example, moisturizers, decongestants, ocular modulators, anti-inflammatory or astringent agents, antihistamines or anti-allergic agents, vitamins, amino acids, antibacterial agents, bactericidal agents, sugars, polysaccharides or their derivatives, cellulose or its derivatives or their salts, water-soluble polymers other than those mentioned above, local anesthetics, steroids, glaucoma treatments, cataract treatments, isotonic agents, buffers, pH adjusters, solubilizers, thickeners (dispersants), stabilizers (antioxidants), and preservatives. These components may be used individually or in combination of two or more.

[0086] To obtain a more sufficient effect in suppressing blue light damage, it is preferable to include a moisturizer in topical preparations used on the eyes. Examples of humectants include: viscosity modifiers such as cellulose-based polymer compounds, vinyl-based polymer compounds and their salts; polysaccharides such as xanthan gum, dextrin, dextran, and heparin; mucopolysaccharides such as hyaluronic acid, sodium hyaluronate, and sodium chondroitin sulfate; polyhydric alcohols such as propylene glycol, 1,3-butylene glycol, polyethylene glycol, and glycerin; sugars such as glucose, trehalose, lactose, and sorbitol; and sugar derivatives of polyhydric alcohols such as glyceryl glucoside. For topical preparations used on the eyes, the preferred moisturizer is a sugar derivative of mucopolysaccharides or polyhydric alcohols, and more preferably sodium hyaluronate or glyceryl glucoside. The amount of moisturizer contained in topical preparations for use on the eyes is not particularly limited, but from the viewpoint of the stability of the topical preparation and its moisturizing effect, 0.1 to 10% by mass is preferred, 0.1 to 5% by mass is more preferred, and 0.3 to 3% by mass is even more preferred.

[0087] There are no particular restrictions on the method of manufacturing topical preparations for use in the eyes, and they can be manufactured using well-known methods. For example, in the case of eye drops, the raw materials can be mixed in a suitable diluent such as distilled water or purified water, adjusted to the desired osmotic pressure and pH, sterilized by autoclaving or filtration under sterile conditions, and then aseptically filled into a cleaned and sterilized container. Alternatively, in the case of eye ointments, for example, a blue light damage inhibitor can be mixed into a commonly used eye ointment base and prepared aseptically according to conventional methods.

[0088] Examples of topical preparations for hair include shampoos, conditioners, hair treatments, hair tonics, hair growth products, hair styling products (hair creams, hair lotions, hair foams, hair mists, etc.), hair colorants, and permanent wave agents. Topical preparations for hair may be rinse-off or leave-in preparations, but leave-in preparations are preferred. Because they are easy to administer, topical preparations for hair are preferably treatments or styling products, more preferably styling products, and even more preferably hair mists.

[0089] The topical preparation for use on hair preferably contains component (A) at a concentration of 0.01 to 2% by mass, more preferably 0.025 to 0.5% by mass, from the viewpoint of suppressing blue light damage. Depending on the amount and length of hair, the topical preparation for use on hair is preferably used at a concentration of 0.5 to 15 g, more preferably 1 to 10 g per day.

[0090] Topical preparations for hair may contain, as needed, ingredients commonly used in hair cosmetics, such as oils and fats, waxes, hydrocarbon oils, ester oils, higher alcohols, silicone oils, UV absorbers, UV scatterers, moisturizers, surfactants, water-soluble polymers, thickeners, powders, skin protectants, whitening agents, wrinkle-improving agents, anti-aging agents, plant extracts, preservatives, anti-inflammatory agents, pH adjusters, metal ion chelating agents, antioxidants, stabilizers, fragrances, dyes, pigments, etc. These ingredients may be used individually or in combination of two or more.

[0091] Since a more sufficient effect in suppressing blue light damage can be obtained, it is preferable to incorporate plant extracts into topical preparations used on hair. Examples of plant extracts include mulberry bark, peony, scutellaria, chamomile, angelica, rosemary, geranium, lithospermum, tea, kudzu root, clove, licorice, loquat, orange peel, ginseng, peony, hawthorn, oak, ginger, pine cone, magnolia, catechu, scutellaria, aloe, marsh marigold, spiraea, watercress, cinchona, comfrey, belladonna, jojoba, gentian, yarrow, almond, cocoa, macadamia nut, olive, ginger, corn, linden, pine, mint, burdock, sesame, prune, houttuynia cordata, bamboo grass, camellia, grapefruit, mallow, rice, avocado, and cactus. Extracts of lavender, sunflower, cypress, sesame, lily, yuzu, rose, acerola, cucumber, rice, shea butter, birch, tomato, garlic, witch hazel, loofah, hops, peach, apricot, lemon, kiwi, houttuynia cordata, chili pepper, Sophora flavescens, dock, water lily, sage, yarrow, mallow, angelica tree, gentian, swertia japonica, thyme, birch, horsetail, loofah, horse chestnut, saxifrage, arnica, lily, mugwort, Phellodendron amurense, safflower, gardenia fruit, jujube, citrus peel, coix seed, gardenia, chamomile, lemon balm, loquat, geranium, heather, horsetail, and hibiscus are among the extracts available. The plant extract to be included in the topical preparation for hair is preferably geranium extract or hibiscus extract, with geranium extract being more preferable. The amount of plant extracts contained in topical preparations for hair is not particularly limited, but from the viewpoint of the stability of the topical preparation, it is preferably 0.01 to 3% by mass as dry solids, more preferably 0.05 to 2% by mass, and even more preferably 0.1 to 1% by mass.

[0092] <Food and beverages> In the present invention, "food and beverages" means anything that is ingested orally or through gastrointestinal administration in daily life, and may include, for example, general food and beverages, health foods, health drinks, supplements, functional foods for health, functional drinks for health, nutritional supplements, nutritional supplement drinks, quasi-drugs, pharmaceuticals (oral medications), etc. One aspect of the present invention is a food or beverage containing the blue light damage suppressing agent, preferably a food or beverage for suppressing blue light damage containing the blue light damage suppressing agent.

[0093] The properties, dosage form, and shape of the food and beverage are not particularly limited and can be appropriately selected according to the purpose. The food and beverage may be solid preparations, liquid preparations, frozen desserts, noodles, confectionery, bread, processed seafood and livestock products, dairy products, processed oils and fats, seasonings, retort pouch foods, etc. Food and beverages are preferably solid or liquid formulations, and more preferably solid formulations, because they are easy to administer and readily exert a blue light damage suppression effect.

[0094] Examples of solid dosage forms include powders, granules, tablets, chewable tablets, capsules, and lozenges, but tablets, chewable tablets, or capsules are preferred.

[0095] In solid dosage forms, auxiliary agents such as excipients, binders, disintegrants, lubricants, fluidizers, flavoring agents, and stabilizers may be used. Suitable examples of excipients in solid dosage forms include lactose, D-mannitol, and starch. Suitable examples of binders include crystalline cellulose, sucrose, D-mannitol, sugar alcohols, dextrin, and hydroxypropylcellulose. Suitable examples of disintegrants include starch, carboxymethylcellulose, and carboxymethylcellulose calcium. Suitable examples of lubricants include magnesium stearate and calcium stearate. Suitable examples of fluidizers include silicon dioxide.

[0096] Liquid preparations include oral solutions, syrups, and drinks, as well as beverages such as fruit juices, teas, cocoa, vegetable juices, green juices, soy milk, dairy drinks, lactic acid drinks, near-water, sports drinks, nutritional drinks, and carbonated drinks.

[0097] The liquid formulation may contain auxiliary components such as solubilizers, suspending agents, isotonic agents, buffering agents, antioxidants, flavorings, seasonings, sweeteners, and thickeners. The solvent should be capable of dissolving component (A) and have high biocompatibility. Suitable examples of solvents include water and ethanol, with water being preferred.

[0098] The amount of ingredient (A) in food and beverages should be appropriately selected depending on the type of food or beverage in question. If the food or beverage is a beverage, the content of component (A) is preferably 0.001 to 3% by mass, more preferably 0.01 to 2% by mass, and even more preferably 0.01 to 1% by mass. When the food or beverage is a solid formulation, the content of component (A) is preferably 0.1 to 30% by mass, more preferably 0.5 to 20% by mass, and even more preferably 1 to 15% by mass. In the case of solid preparations such as capsules, which are taken orally without much of component (A) dissolving into the oral cavity, the content of component (A) is preferably 10 to 95% by mass, more preferably 30 to 90% by mass, and even more preferably 50 to 85% by mass. [Examples]

[0099] The present invention will now be described in more detail with reference to examples, but the present invention is not limited thereto.

[0100] [Example 1] Effects of blue light irradiation on normal human skin cells (Preparation of test substance) The test substances used were αG rutin (α-glucosylrutin), αG hesperidin (α-glucosyl hesperidin), and αG naringin (α-glucosylnaringin). The composition of each test substance is as follows. αG-rutin (αG-rutin PS-C, manufactured by Toyo Sugar Refining Co., Ltd.): α-monoglucosylrutin 65% by mass, isoquercitrin 15% by mass αG-Hesperidin (αG-Hesperidin PS-CC, manufactured by Toyo Sugar Refining Co., Ltd.): α-Monoglucosylhesperidin 80% by mass, 7-Glucosylhesperetin 10% by mass αG-naringin (Enzyme-treated naringin): α-monoglucosylnaringin 75% by mass, 7-glucosylnaringenin 10% by mass 500 mg of each test substance was diluted to 10 mL with deionized water to prepare a stock solution. This stock solution was then progressively diluted with deionized water to prepare a dilution series for each test substance. Each dilution series of the test substance was added to the culture medium at a volume of 1 / 1000.

[0101] (Cell culture and blue light irradiation) Epidermal keratinocytes (from adult, manufactured by KURABO, NO. KK-4109) were placed in a 96-well plate in a 2x10⁶ arrangement. 4 Cells were seeded in a cell / well and incubated at 37°C under 5% CO2. HuMedia-KG2 (KURABO, NO. KK-2150S) was used as the culture medium. 24 hours after seeding, the medium was replaced with one containing only the test substance or solvent, and the cells were cultured for 1 hour. Subsequently, the cells were cultured for 18 hours in the incubator while irradiating the cell culture surface with a blue LED (BioResearch Center Co., Ltd., LEDA-420, peak wavelength 420 nm) to an illuminance of 500 lx. Illuminance was measured using a light meter (Kenis Corporation, UV-340A). As a control, cells cultured in a medium containing only the solvent were cultured without blue light irradiation. Experiments were conducted with N=3 per experimental condition.

[0102] (Measurement of the number of viable cells) After washing the 96-well plate with PBS, the absorbance at 450 nm was measured using a microplate reader with a Cell Counting Kit-8 (DOJINDO, NO.CK04). Cell Counting Kit-8 uses tetrazolium salt as a chromogenic substrate. Tetrazolium salt is reduced to orange, water-soluble formazan by NADH produced by dehydrogenases in cells, so the amount of formazan is proportional to the number of viable cells. The number of viable cells can be measured by measuring the absorbance of formazan at 450 nm. The percentage of living cells (%) was calculated using the following formula (I). Live cells (%) = (Absorbance of the test group irradiated with blue light for each test substance) / (Absorbance of the test group not irradiated with blue light) × 100 ... Equation (I) The p-value was calculated using the control group with blue light irradiation but no sample addition (0 ppm), and a p-value of < 0.05 was considered statistically significant (*).

[0103] (result) The results are shown in Figures 1 to 4. In the figures, BL(-) indicates no blue light irradiation, BL(+) indicates blue light irradiation, and "no additive" indicates that only the solvent was added. The vertical axis of the graph shows the cell viability (%). Figure 1 shows that αG-rutin suppresses blue light-induced damage at concentrations of 0.00625%, 0.0125%, 0.025%, and 0.05%. The blue light-induced damage suppression effect of αG-rutin was concentration-dependent, and was particularly significant at concentrations of 0.0125% and 0.05%. Figure 2 shows that αG hesperidin significantly suppressed blue light-induced damage at concentrations of 0.25% and 0.5%. Figure 3 shows that αG-naringin significantly suppressed blue light-induced damage at concentrations of 0.025% and 0.05%. Figure 4 clearly shows that among αG-rutin, αG-hesperidin, and αG-naringin, αG-rutin had the highest effect in suppressing blue light damage.

[0104] [Reference Example 1] Measurement of the absorption spectrum of the test substance (method) The same test substances were used as in Example 1. Each test substance was dissolved in deionized water to prepare aqueous solutions with a final concentration of 20 ppm for αG rutin, and 25 ppm each for αG hesperidin and αG naringin. An aqueous solution of the test substance was placed in a quartz cell (cell length 10.0 mm), and the absorption spectrum from 200 nm to 900 nm was measured using a spectrophotometer (Hitachi High-Tech Science Corporation, NO.U-3900).

[0105] (result) The absorption spectra of αG-rutin, αG-hesperidin, and αG-naringin in the 200nm to 500nm range are shown in Figures 5 to 7, respectively. Figure 5 clearly shows that αG-rutin hardly absorbs light in the blue light wavelength range (400nm-500nm). Figure 6 clearly shows that αG hesperidin does not absorb light in the blue light wavelength range (400nm-500nm). Figure 7 clearly shows that αG-naringin does not absorb light in the blue light wavelength range (400nm-500nm). From these results, it became clear that the blue light damage suppression effect of αG-rutin, αG-hesperidin, and αG-naringin is not due to the absorption of blue light wavelengths (400nm-500nm) by αG-rutin, αG-hesperidin, and αG-naringin, but rather to an effect due to a mechanism other than that described above.

[0106] [Reference Example 2] Measurement of the spectral distribution of a blue LED (method) In Example 1, the spectral spectrum of the blue LED used for blue light irradiation was measured using a measurement system consisting of a visible-range engraved diffraction grating (manufactured by Thorlabs) and an optical power meter (manufactured by BRC BioResearch Center).

[0107] (result) The results are shown in Figure 8. The peak wavelength was 420 nm.

[0108] [Examples 2-34] Skin cream, face cream, eye cream, lotion, serum, drink, tea beverage, eye drops, hair mist, capsules, and chewable tablets were prepared by weighing and mixing each component according to the proportions listed in Tables 1 to 11.

[0109] [Table 1]

[0110] [Table 2]

[0111] [Table 3]

[0112] [Table 4]

[0113] [Table 5]

[0114] [Table 6]

[0115] [Table 7]

[0116] [Table 8]

[0117] [Table 9]

[0118] Table 10

[0119] Table 11

Claims

1. A blue light damage inhibitor containing α-glucosylrutin, which suppresses damage caused by blue light to cells constituting the skin or eyes, The cells constituting the skin or eye are epidermal keratinocytes or corneal epithelial cells, A blue light damage inhibitor in which the aforementioned damage is cell death of cells constituting the skin or eyes.

2. The blue light damage inhibitor according to claim 1, wherein the α-glucosylrutin comprises α-monoglucosylrutin.

3. The blue light damage inhibitor according to claim 1 or 2, wherein the α-glucosylrutin content is 65% by mass or more.

4. A topical preparation or food / beverage for inhibiting blue light damage, used on the skin or eyes, comprising the blue light damage inhibitor described in any one of claims 1 to 3.

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