Multi-channel synergistic anti-blue-light targeted repair composition, skin care product and preparation method
Through the multi-pathway synergistic effects of siRNA liposomes, resveratrol and α-arbutin, a temporal network of gene regulation, enzyme activity inhibition and pigment metabolism intervention units is constructed, which solves the problems of single protection and insufficient time effect of existing anti-blue light skin care technology, and realizes comprehensive skin damage repair and protection.
Patent Information
- Application Number
- CN202510752838.4
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2025-06-06
- Publication Date
- 2025-09-12
AI Technical Summary
Existing anti-blue light skin care technology has the problems of a single protection dimension, insufficient duration of action, lack of multi-dimensional protection and targeted repair capabilities, and low efficiency of active ingredients in transdermal penetration, making it difficult to form a cyclical protection system that runs through immediate protection and continuous repair.
A multi-pathway synergistic anti-blue light targeted repair composition is used, including siRNA liposomes, resveratrol and α-arbutin in a specific proportion. By constructing a temporal synergistic network of gene regulatory units, enzyme activity inhibition units and pigment metabolism intervention units, the source of damage signals is cut off and the damage process is dynamically repaired. Liposome encapsulation technology is used to improve the transdermal efficiency and stability of active ingredients.
It achieves multi-dimensional and all-round anti-blue light damage effects, effectively resists the damage of blue light to the extracellular matrix of the skin, regulates abnormal pigment metabolism, relieves inflammatory responses, and provides comprehensive and lasting protection and repair.
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Figure CN120617079A_ABST
Abstract
Description
Technical Field
[0001] The present invention relates to the field of cosmetics, and in particular to a multi-pathway synergistic anti-blue light targeted repair composition, a skin care product and a preparation method. Background Art
[0002] With the changes in modern lifestyles, people's exposure to electronic devices has increased significantly, and the damage caused by blue light to the skin has become a major concern in the field of skin health. Blue light is high-energy visible light with a wavelength between 400-480nm. It has strong penetrating and oxidizing capabilities. Although its energy is lower than ultraviolet rays, it can act on the skin at close range for a long time through devices such as electronic screens, causing cumulative damage to multiple targets. The specific mechanism is as follows: blue light penetrates the epidermis directly into the dermis, inducing photooxidative stress response, activating matrix metalloproteinases (MMPs) to degrade collagen, triggering a cascade of inflammatory factors, and disrupting the pigment metabolism pathway, ultimately causing skin aging, sagging, pigmentation and sensitivity symptoms.
[0003] At present, anti-blue light skin care technologies mainly include three categories: physical protection, chemical protection, and bioactive ingredient repair. Among them, physical protection mainly forms a physical barrier by adding inorganic particulate matter such as titanium dioxide and zinc oxide to reflect or scatter blue light. However, this type of protection often has problems such as a narrow protection band and a thick skin feel, which makes it difficult to meet the needs of daily use. Chemical protection converts light energy into heat energy by adding organic molecules that can absorb light of specific wavelengths, such as troxerutin and ferulic acid. CN111150670B discloses an anti-ultraviolet and anti-blue light liquid crystal nanolipid liquid, which contains ingredients such as troxerutin, ferulic acid, resveratrol, and baicalin, which can resist the hazards of ultraviolet and blue light in all bands. However, the effect of this type of chemical protection ingredient is short-lived and cannot block the conduction of downstream damage signals. Bioactive ingredient repair technology has been a hot topic of research in recent years, mainly by adding antioxidant ingredients, cell protection ingredients, etc. to reduce the oxidative stress response caused by blue light. CN113069392A discloses a blue light-resistant skin care composition. Combining multiple components, including calendula extract, active small molecule peptides, and niacinamide, it boasts a strong antioxidant effect, effectively alleviating oxidative stress caused by blue light pollution. CN119097571A provides a liposome-based skin care composition that encapsulates multiple active ingredients to improve their stability and permeability, enhancing skin care effectiveness.
[0004] However, current anti-blue light technologies have significant limitations, mainly manifested in a single dimension of protection and insufficient duration of action. Although physical protective measures (such as sunscreens containing mineral powders) can reflect some blue light, they have problems such as a narrow protection band and a thick feel on the skin; although chemical protective ingredients (such as antioxidants) can neutralize reactive oxygen species induced by blue light, their duration of action is short and they cannot block downstream damage signal transduction; although biologically active ingredients (such as peptide inhibitors) can target and inhibit specific enzyme activity, the lack of regulation at the genetic level leads to a delayed protective effect. More importantly, existing technologies mostly adopt an isolated action mode, lacking synergistic intervention in the three major pathways of photoaging, inflammatory response and pigmentation, and the low transdermal efficiency of active ingredients leads to insufficient concentration at the action site, making it difficult to form a cyclical protection system that runs through "immediate protection-continuous repair".
[0005] This technological landscape presents a key challenge for the development of blue light protection products: how to provide effective, multi-dimensional protection and targeted repair capabilities while maintaining user comfort. Current solutions on the market often focus on intervening in a single damage pathway: for example, by adding antioxidants to neutralize free radicals or relying on physical reflectors to disperse light energy. However, these approaches overlook the cascade of blue light damage, from ROS generation, abnormal gene expression, to extracellular matrix degradation. This fragmented protection strategy not only wastes resources but also potentially diminishes effectiveness due to interference between different mechanisms of action. Summary of the Invention
[0006] The purpose of the present invention is to overcome the defects of the above-mentioned prior art and provide a multi-pathway synergistic anti-blue light targeted repair composition, skin care product and preparation method. Based on the three-dimensional protection model of "signal blocking-matrix protection-metabolic regulation", by constructing a temporal synergistic network of gene regulatory units, enzyme activity inhibition units and pigment metabolism intervention units, the source of damage signals is cut off and the damage process is dynamically repaired, thereby achieving a multi-dimensional and comprehensive anti-blue light damage effect.
[0007] The purpose of the present invention can be achieved through the following technical solution: a multi-pathway synergistic anti-blue light targeted repair composition, which comprises siRNA liposomes, resveratrol and α-arbutin in a mass ratio of (0.01-5): (0.01-5): (0.01-3).
[0008] Furthermore, the mass ratio of the siRNA liposome, resveratrol, and α-arbutin is (3-5): (1-5): (1-3).
[0009] Furthermore, the preparation method of the siRNA liposome is:
[0010] (1) Dissolve the phospholipids fully in ethanol. After the phospholipids are fully dissolved, evaporate the ethanol at low temperature to form a uniform phospholipid film.
[0011] (2) Stir and mix the phosphate buffer solution and siRNA;
[0012] (3) adding the mixed solution obtained in step (2) to the phospholipid membrane of step 1), wherein the mass ratio of the mixed solution to the phospholipid of step (1) is 5:1 to 10:1, and performing water-treatment on the phospholipid membrane. After the phospholipid membrane is completely detached, performing ultrasonic treatment to obtain functional liposomes.
[0013] Furthermore, in step (1), the mass volume ratio of phospholipid to ethanol is (1-5): (5-50) mg / mL.
[0014] Furthermore, in step (2), the mass volume ratio of siRNA to phosphate buffer solution is (100-500): (20-50) mg / mL. The present invention also provides a skin care product, comprising a matrix excipient and an effective ingredient, wherein the effective ingredient comprises the composition, and the weight percentage of the composition in the skin care product is 0.03-13%.
[0015] Furthermore, the matrix excipients include phase A excipients, phase B excipients, phase C excipients and phase D excipients;
[0016] Taking the weight parts of the skin care product as 100 parts,
[0017] The phase A auxiliary material includes 0.05-5 parts of a thickener, 0.11-3 parts of a skin conditioner, and 3.6-10 parts of a moisturizer;
[0018] The phase B auxiliary material includes 0.4-4 parts of a softener and 0.6-3 parts of an emulsifier;
[0019] The phase C auxiliary material includes 0.1 to 3 parts of a pH regulator;
[0020] The phase D auxiliary material includes 0.1 to 2 parts of fragrance and 0.02 to 2 parts of preservative.
[0021] Further, the thickener includes one or more of cetyl ethylhexanoate, xanthan gum, acrylates / stearyl alcohol polyether-20 methacrylate copolymer, acrylates / C10-30 alkyl acrylate crosspolymer, tamarindus indica seed polysaccharide, sodium acrylate / sodium acryloyldimethyl taurate copolymer, octyldodecanol, cetearyl dimethicone / vinyl dimethicone crosspolymer and acrylamide / sodium acryloyldimethyl taurate copolymer;
[0022] The skin conditioning agent includes one or more of sodium hyaluronate, hydrolyzed sodium hyaluronate, allantoin, niacinamide, tocopheryl acetate, bisabolol, shea butter (BUTYROSPERMUM PARKII) and lavender oil (LAVANDULA ANGUSTIFOLIA);
[0023] The moisturizing agent includes one or more of glycerin, propylene glycol, butylene glycol, panthenol, inositol, hyaluronic acid, β-glucan, glucose, hydrogenated lecithin, mannitol and erythritol;
[0024] The emollient comprises one or more of dimethicone, caprylic / capric triglyceride, phytosteryl / octyldodecanol lauroyl glutamate, glyceryl stearate, cyclopentasiloxane, ethylhexyl palmitate, squalane, trehalose, mineral oil, glyceryl caprylate, soybean (Glycine Max) oil, jojoba (SIMMONDSIA CHINENSIS) seed oil, raspberry (RUBUS IDAEUS) seed oil, caprylyl glycol, isononyl isononanoate, isohexadecane, meadowfoam (LIMNANTHES ALBA) seed oil, dimethiconol and olive (OLEA EUROPAEA) fruit oil;
[0025] The emulsifier includes one or more of cetearyl alcohol, glyceryl stearate, PEG-30 hydrogenated castor oil, PEG-40 hydrogenated castor oil, PEG-100 stearate, cetearyl glucoside, polysorbate-20, polysorbate-80, polysorbate-60, ethylene glycol distearate, sorbitan stearate, sorbitan isostearate, sorbitan oleate, polyglyceryl-2 triisostearate and PEG-150 distearate;
[0026] The pH regulator includes one or more of citric acid, sodium citrate, arginine and lactic acid;
[0027] The aromatic agent includes essence;
[0028] The preservatives include one or more of methylparaben, propylparaben, phenoxyethanol, ethylhexylglycerin and pentylene glycol.
[0029] The present invention also provides a method for preparing the above-mentioned skin care product, comprising the following steps:
[0030] a. Aqueous phase: After fully moistening and mixing the components of phase A excipients, add them to water, stir thoroughly until completely dissolved, and heat;
[0031] b. Oil phase; mix and heat the B phase excipients, stirring until completely dissolved;
[0032] c. Emulsification: Add the mixture from step b to the aqueous phase from step a, stirring and homogenizing;
[0033] d. Add phase C auxiliary material, stir and homogenize, and cool to 40-50℃;
[0034] e. Add phase D auxiliary material and stir;
[0035] f. After stirring and cooling to 35-38 ° C, add the effective ingredient composition E, stir and homogenize to obtain the product.
[0036] Furthermore, the heating temperature in steps a to b is 75 to 85°C;
[0037] The stirring speed in steps c to f is 200 to 400 rpm, and the stirring time is 3 to 10 minutes;
[0038] The homogenization speed in steps c to f is 2000 to 4000 rpm, and the homogenization time is 3 to 5 minutes.
[0039] Compared with the prior art, the present invention has the following beneficial effects:
[0040] 1. The present invention aims to provide a composition that achieves resistance to blue light damage through multi-pathway synergy. The composition contains siRNA, resveratrol and α-arbutin, which can effectively resist the damage of blue light to the extracellular matrix of the skin, regulate abnormal pigment metabolism, alleviate inflammatory response, achieve multi-dimensional and comprehensive anti-blue light damage effect, and provide comprehensive and long-lasting protection and repair for the skin.
[0041] The technical solution of this invention is based on a three-dimensional protection model of "signal blocking-matrix protection-metabolic regulation," breaking through the limitations of traditional single-pathway intervention and constructing a systematic solution for anti-blue light skincare. siRNA, as the core of gene regulation, targets and silences key damage genes such as MMP-1 and IL-6 through the RNA interference mechanism, blocking the inflammatory cascade to achieve signal blockade and inhibiting collagen degradation to maintain matrix integrity. Resveratrol, as a multi-functional active ingredient, not only exerts an antioxidant effect by scavenging ROS to block oxidative stress signals, but also participates in metabolic regulation and promotes damage repair through its anti-inflammatory properties. α-Arbutin, as a tyrosinase inhibitor, reduces melanin synthesis by blocking dopaquinone production, directly intervening in the pigment metabolism pathway.
[0042] 2. This invention utilizes liposome encapsulation technology to significantly enhance the transdermal efficiency and stability of the active ingredient, enabling it to form a long-lasting concentration gradient across the epidermis and dermis, achieving a comprehensive "protection-repair" approach. This multi-target synergistic composition addresses the blind spots of existing technologies and provides a systematic solution for anti-blue light skincare. BRIEF DESCRIPTION OF THE DRAWINGS
[0043] Figure 1 The skin texture before and after using the essence of Example 3, where A is the skin texture before using the essence of Example 3, B is the skin texture after using the essence of Example 3 for two weeks, and C is the skin texture after using the essence of Example 3 for four weeks. DETAILED DESCRIPTION
[0044] The present invention is described in detail below with reference to specific embodiments.
[0045] Based on a three-dimensional protection model of "signal blocking - matrix protection - metabolic regulation," this invention uses a specific ratio of siRNA, resveratrol, and α-arbutin to work synergistically. By constructing a sequential collaborative network of gene regulation units, enzyme activity inhibition units, and pigment metabolism intervention units, it achieves the source of damage signal truncation and dynamic repair of the damage process. Specific details are as follows:
[0046] siRNA (small interfering RNA) is a double-stranded RNA molecule that precisely regulates gene expression through the RNA interference (RNAi) mechanism. Its action begins when the double strands of siRNA dissociate after entering the cell. The released antisense strand binds to the RNA-induced silencing complex (RISC) to form an active complex, which then targets and degrades specific mRNA through complementary base pairing, thereby blocking the synthesis of related proteins. In the field of anti-blue light skin care, siRNA, based on its gene silencing properties, comprehensively resists blue light damage through a multi-dimensional intervention mechanism: by targeting and silencing the matrix metalloproteinase MMP-1 gene, it directly inhibits collagen decomposition and improves blue light-induced skin structure relaxation; by degrading the mRNA of the inflammatory factor IL-6, it blocks the activation of the NF-κB signaling pathway, and alleviates the inflammatory response and sensitivity problems caused by blue light from the root; at the same time, by precisely cutting tyrosinase (TYR) mRNA, it inhibits the activation of the melanin synthesis pathway and prevents abnormal pigmentation caused by blue light. siRNA (small interfering RNA) is a synthetic double-stranded RNA molecule composed of a sense and antisense strand that form a stable double-stranded structure through complementary base pairing. It is typically 21-23 nucleotides in length. Its sequence is designed to precisely match the target gene's mRNA and is widely used to specifically silence or downregulate target gene expression. Mechanistically, siRNA achieves efficient gene regulation through RNA interference (RNAi): First, siRNA enters target cells (such as melanocytes and fibroblasts) with the help of a delivery system. Inside the cell, the double-stranded structure dissociates, and the antisense strand binds to the RNA-induced silencing complex (RISC) to form an active complex. Subsequently, the RISC-siRNA complex specifically recognizes and binds to the target gene mRNA, inducing ribonuclease (RNase) to degrade the mRNA, thereby blocking the translation of the target gene. In the field of anti-blue light skincare, siRNA achieves deep intervention in photodamage pathways through multi-target coordinated design. It targets the MMP-1 gene to inhibit collagen degradation, inhibits IL-6 expression to block the inflammatory cascade, and regulates melanin synthesis from the source by degrading tyrosinase (TYR) mRNA. Compared to traditional single-pathway inhibitors, siRNA gene-level regulation can simultaneously act on the generation, transmission, and effect stages of damage signals, forming a multi-dimensional protection network and achieving systemic defense and repair against blue light damage. Currently commercially available siRNAs can be used in this invention, such as those sold by Wuhan Zhongke Optical Valley Technology Co., Ltd.
[0047] Resveratrol is a naturally occurring polyphenol compound, mainly derived from plants such as peanuts, grapes, Japanese knotweed, and mulberries. As a powerful natural antioxidant, it has multiple biological activities and skin care effects. In anti-blue light targeted repair skin care products, its mechanism of action is mainly reflected in two aspects: on the one hand, resveratrol exerts an antioxidant effect by scavenging free radicals, protecting cells from blue light-induced oxidative damage; on the other hand, resveratrol effectively blocks its damage to the extracellular matrix by targeted inhibition of MMP-1 activity, thereby maintaining the structural integrity of the skin, delaying the photoaging process, and reducing wrinkles and sagging. In addition, resveratrol also has anti-inflammatory effects, can reduce skin inflammatory reactions, relieve redness, swelling, sensitivity and other problems; at the same time, it can promote the repair of skin damage caused by ultraviolet radiation such as blue light, improve skin texture and appearance, and provide comprehensive protection and repair for the skin. Currently available resveratrol can be used in the present invention, such as the SC-006 model resveratrol sold by Guangzhou Taikang Daily Chemical Co., Ltd. and Xi'an Shangcheng Biotechnology Co., Ltd.
[0048] α-Arbutin is a natural glycoside derivative, mainly extracted from the leaves of the Ericaceae plant bearberry. As a competitive tyrosinase inhibitor, α-arbutin can accurately occupy the active center of tyrosinase, block the production of dopaquinone, and then reduce the synthesis of melanin, achieving the effect of whitening and lightening spots. At the same time, α-arbutin can also scavenge reactive oxygen species (ROS) induced by blue light, inhibit lipid peroxidation, and protect the integrity of mitochondrial membrane potential, thereby exerting a powerful antioxidant defense effect and helping the skin resist oxidative stress damage caused by blue light. Currently available α-arbutin can be used in the present invention, such as the DNS-XGG98 model α-arbutin sold by Shaanxi Dennis Biotechnology Co., Ltd. and the α-arbutin sold by Xi'an Lanshan Biotechnology Co., Ltd. The present invention works through synergistic effects at multiple levels:
[0049] Highly efficient gene regulation technology: Utilizing siRNA (small interfering RNA) technology, efficient gene regulation is achieved through the RNA interference (RNAi) mechanism. siRNA can precisely match and silence or downregulate the expression of target genes, thereby blocking the generation, transmission, and effect stages of blue light damage signals.
[0050] Break through the single protection mechanism and achieve full-chain damage blocking:
[0051] Existing technologies only respond to blue light damage through a single pathway (such as antioxidant or physical barrier), while the present invention constructs a three-dimensional protection model of "signal blocking-matrix protection-metabolic regulation":
[0052] Genetic level: Use siRNA technology to target and silence MMP-1 and IL-6 genes, blocking collagen degradation and inflammatory cascade reactions from the source.
[0053] Enzyme activity level: Resveratrol forms a dual antioxidant protection by inhibiting MMP-1 activity and scavenging free radicals.
[0054] Metabolic level: α-Arbutin inhibits tyrosinase activity and regulates abnormal pigment metabolism. This multi-target synergistic mechanism expands the protection dimension from a single link to the entire chain of blue light damage.
[0055] Furthermore, this invention utilizes liposome encapsulation technology to significantly enhance the transdermal efficiency and stability of the active ingredient, enabling it to form a long-lasting concentration gradient across the epidermis and dermis, achieving comprehensive "protection-repair" management. Through multi-target synergy, this composition addresses the blind spots of existing technologies and provides a systematic solution for anti-blue light skincare.
[0056] The raw materials and detection methods involved in the present invention are commonly used in the art unless otherwise specified.
[0057] The composition of the present invention that achieves resistance to blue light damage through multi-pathway synergistic action can be used in skin care products. The skin care products can be any form of skin care products or cosmetics, including skin care water, essence, lotion, cream, mask, freeze-dried powder, etc.
[0058] Each experiment was conducted using essence as an example, but the present invention is not limited to the use of essence. The essence of the present invention comprises a matrix excipient and an effective ingredient, wherein the effective ingredient comprises a composition that achieves resistance to blue light damage based on multi-pathway synergy. Specifically, the composition of the purified solution is shown in Table 1 below:
[0059] Table 1 Composition of the essence
[0060]
[0061]
[0062] The siRNA liposomes used in the following examples were prepared by the following method:
[0063] (1) Dissolve phospholipids in ethanol, stir until fully dissolved, and then transfer to a rotary evaporator to remove ethanol at low temperature to form a uniform phospholipid film on the bottom surface of the container; the mass volume ratio of phospholipids to ethanol is 3:50 mg / mL;
[0064] (2) Stirring the phosphate buffer solution and siRNA until evenly mixed; the mass volume ratio of siRNA to phosphate buffer solution is 400:50 mg / mL;
[0065] (3) adding the mixed solution obtained in step (2) to the rotary evaporator of step 1), wherein the mass ratio of the mixed solution to the phospholipid of step (1) is controlled to be 5:1, and the phospholipid film is treated with water. After the phospholipid film is completely detached, ultrasonic treatment is performed to obtain functional liposomes.
[0066] The above-mentioned skin care product is prepared by the following method:
[0067] a. Water phase: Place water in a container with a stirring device and stir. After fully moistening and mixing the other components of Phase A excipients, add them to the water, stir thoroughly until completely dissolved, and heat to 75-80°C;
[0068] b. Oil phase; mix the components of phase B excipients, heat to 75-85°C, and stir until completely dissolved;
[0069] c. Emulsification: The oil phase obtained in step b is added to the aqueous phase obtained in step a, stirred at 200-400 rpm for 3-5 min, and then homogenized at 2000-4000 rpm for 3-5 minutes;
[0070] d. Add phase C auxiliary material, stir at 200-400rpm for 3-5min, then homogenize at 2000-4000rpm for 3-5 minutes, and cool to 40-50℃ with stirring;
[0071] e. Add phase D auxiliary material and stir at 200-400 rpm for 5-10 minutes;
[0072] All the above steps are strictly controlled for sterility;
[0073] g. After stirring and cooling to 35-38°C, add the active ingredient composition E, stir at 200-400 rpm for 3-5 minutes, and then homogenize at 2000-4000 rpm for 3-5 minutes to obtain the desired essence. Filter and sterilize before filling, and test the bacterial content, toxins, and immunogenicity for quality control.
[0074] Example
[0075] The following is a detailed description using essence as an example, that is, the skin care products in each embodiment and comparative example are essences.
[0076] (1) The specific formula is shown in the following table:
[0077] Table 2 Raw material composition formula of Examples 1-3 and Comparative Examples 1-6 and Blank Examples (weight percentage %)
[0078]
[0079]
[0080] The only difference between Example 2 and Example 1 is the increase of each active ingredient, and the only difference between Example 3 and Example 1 is the reduction of each active ingredient.
[0081] The difference between Comparative Examples 1-3 and Example 3 is that only one key composition component is missing, the difference between Comparative Examples 4-6 and Example 3 is that only two key composition components are missing, and the difference between Blank Example 1 and Example 3 is that all key composition components are missing.
[0082] The specific ratios are shown in Table 2, and the preparation method is the same as that in Example 1.
[0083] (2) According to the dosage of each component of Examples 1-3, Comparative Examples 1-6 and the blank in Table 2, an essence was prepared by the following method:
[0084] a. Water phase: Place water in a container with a stirring device and stir. After fully moistening and mixing the other components of Phase A excipients, add them to the water, stir thoroughly until completely dissolved, and heat to 80°C.
[0085] b. Oil phase; mix the components of phase B excipients, heat to 85°C, and stir until completely dissolved;
[0086] c. Emulsification: The oil phase obtained in step b was added to the aqueous phase obtained in step a, stirred at 300 rpm for 5 min, and then homogenized at 3500 rpm for 5 minutes;
[0087] d. Add phase C, stir at 300 rpm for 5 min, then homogenize at 3000 rpm for 3 minutes, stirring and cooling to 45 ° C;
[0088] e. Add phase D auxiliary material and stir at 300 rpm for 10 min;
[0089] All the above steps were strictly controlled for sterility.
[0090] g. After stirring and cooling to 35-38°C, add the active ingredient composition E, stir at 300 rpm for 5 minutes and homogenize at 3000 rpm for 3 minutes to obtain the desired essence. Filter and sterilize before filling, and test the bacterial content, toxins, and immunogenicity for quality control.
[0091] Efficacy evaluation test
[0092] 1. Test of the regulatory effect of the anti-blue light composition on skin fibroblast inflammation and matrix degradation related factors
[0093] Prepare the raw materials according to the ratio in Table 3 below and mix them to obtain the experimental samples:
[0094] Table 3 Cell experiment raw material composition ratio (unit: μg)
[0095]
[0096] Test method for the regulatory effect of the anti-blue light composition on skin fibroblast inflammation and matrix degradation related factors:
[0097] 1) Fibroblasts were cultured at 10 3 -10 4 The cells were seeded at a density of 100 cells / well in a 24-well plate, 200 μL of commercially available DMEM medium was added, and the cells were cultured in a 37° C., 5% CO 2 incubator for 24 hours.
[0098] 2) The samples of Experimental Examples 1-3, Comparative Examples 1-6 and Blank Example 1 were added to the plate and incubated in an incubator for 24 hours.
[0099] 3) The cell culture supernatants were collected and the supernatants of Experimental Examples 1-3, Comparative Examples 1-6 and Blank Example 1 were added to the corresponding reaction wells of an ELISA plate using an ELISA kit for subsequent ELISA analysis.
[0100] The ELISA kit includes MMP-1, IL-6 specific antibodies and standards.
[0101] 4) Measure the absorbance at 450 nm using a microplate reader and calculate the concentrations of MMP-1 and IL-6 in the sample based on the standard curve.
[0102] 5) Using Blank Example 1 as a reference, the inhibition rates of MMP-1 and IL-6 synthesis for Experimental Examples 1-3 and Comparative Examples 1-6 were calculated: Synthesis inhibition rate (%) = (absorbance of test group - absorbance of Blank Example 1) / absorbance of Blank Example 1 * 100%. The test results are shown in Tables 4-5 below.
[0103] Table 4 MMP-1 synthesis inhibition rate
[0104] sample MMP-1 synthesis inhibition rate % Experimental Example 1 50.31 Experimental Example 2 55.85 Experimental Example 3 44.26 Comparative Experimental Example 1 31.09 Comparative Example 2 29.84 Comparative Experiment 3 27.17 Comparative Experiment 4 21.42 Comparative Experimental Example 5 20.25 Comparative Experimental Example 6 14.78 Experimental blank example 1 0.00
[0105] Table 5 IL-6 inhibition rate
[0106] sample IL-6 synthesis inhibition rate% Experimental Example 1 62.17 Experimental Example 2 65.35 Experimental Example 3 58.56 Comparative Example 1 43.29 Comparative Example 2 40.31 Comparative Experiment 3 37.64 Comparative Example 4 25.18 Comparative Experimental Example 5 23.57 Comparative Experimental Example 6 17.32 Experimental blank example 1 0.00
[0107] As can be seen from Tables 4-5, the anti-blue light composition (Experimental Examples 1-3) has a significant inhibitory effect on MMP-1 gene expression and IL-6 synthesis. Specifically, the synthesis inhibition rates of MMP-1 and IL-6 in Experimental Example 1 were 50.31% and 62.17%, respectively, which were significantly better than those in the control example. Further increasing the concentration of the active ingredient (Experimental Example 2) showed a higher inhibitory effect (MMP-1: 55.85%, IL-6: 65.35%), indicating that the content of the active ingredient in the composition is positively correlated with its inhibitory effect, verifying the dose-dependent effect.
[0108] Further comparison of the experimental comparative data shows that the lack of any core component (experimental comparative examples 1-3) or two components (experimental comparative examples 4-6) leads to a significant decrease in the inhibition rate, confirming the necessity of multi-pathway synergy. Specifically, experimental comparative examples 1-3 lack one of the components in siRNA liposomes, resveratrol and α-arbutin, respectively, and their inhibition rates decreased by 15.27%, 18.25% and 20.92% compared to experimental example 3. Experimental comparative examples 4-6 lack two components at the same time, and their inhibition rates decreased by a greater margin, decreasing by 33.38%, 34.99% and 41.24% respectively. It is proved that synergy occurs between the components in the composition, indicating that only a complete combination of ingredients can exert the best anti-blue light effect.
[0109] 2. Melanin synthesis inhibition experiment
[0110] Model: B16-F10 melanocytes
[0111] Test method:
[0112] 1) B16 cell culture and grouping
[0113] Mouse melanoma B16 cells were cultured in DMEM high-glucose medium (pH = 7.2) supplemented with 10% fetal bovine serum and penicillin-streptomycin (100 kU·L-1) at 37°C, 5% CO2, and relative humidity. Cells in the logarithmic growth phase were used for subsequent experiments.
[0114] 2) Determination of intracellular tyrosinase activity
[0115] B16 cells were taken at a rate of 5×10 7 ·L -1 Inoculate into 12-well plates, 1 mL per well, and culture for 24 h. Add 0.2 μmol·L -1 α-MSH was induced to construct a melanin high-expression cell model. The experimental raw material solution of Experimental Examples 1-3, Experimental Comparative Examples 1-6 and Experimental Blank Example 1 was used in turn. Each group had 4 replicate wells. After culturing for 48 hours, the supernatant was discarded and the cells were washed 3 times with PBS. 500 μL of PBS buffer containing 1% TritonX-100 was added to each well and placed in a -80°C refrigerator for 1 hour. Then, the cells were thawed at room temperature and the cell lysate was centrifuged at 12000 r·min. -1 , centrifuge at 4 ° C for 20 min, collect the supernatant. Take 60 μL of the supernatant into a 96-well plate, add 140 μL of 5 mmol·L -1Incubate with L-Dopa at 37°C for 1 hour, and measure the absorbance of each well at 405 nm. Determine the protein content in the solution using the Bradford method. Calculate the relative intracellular tyrosinase activity using the following formula: Relative intracellular tyrosinase activity / % = tyrosinase activity per gram of protein in the experimental group / tyrosinase activity per gram of protein in the α-MSH model group × 100%.
[0116] Table 6 Tyrosinase activity inhibition rate
[0117] sample Tyrosinase activity inhibition rate% Experimental Example 1 81.74 Experimental Example 2 85.62 Experimental Example 3 76.22 Comparative Example 1 55.28 Comparative Example 2 57.74 Comparative Experiment 3 52.13 Comparative Experiment 4 42.85 Comparative Experimental Example 5 38.27 Comparative Experimental Example 6 40.46 Experimental blank example 1 0.00
[0118] As shown in Table 6, Experimental Examples 1 and 3 have a significant inhibitory effect on tyrosinase activity and can reduce the production of melanin. Specifically, the tyrosinase activity inhibition rates of Experimental Examples 1, 2, and 3 reached 81.74%, 85.62%, and 76.22%, respectively. This indicates that as the concentration of the composition increases, its inhibitory effect on tyrosinase activity also increases significantly, showing a dose-dependent effect.
[0119] Further comparison of the experimental comparative data shows that the lack of any core component (experimental comparative examples 1-3) leads to a significant decrease in inhibition rate. Specifically, experimental comparative examples 1-3 lack one of the components of siRNA liposomes, resveratrol and α-arbutin, respectively, and their inhibition rates decreased by 20.94%, 18.48% and 24.09% compared to experimental example 3. Experimental comparative examples 4-6 lack two components at the same time, and their inhibition rates decreased by a greater margin, decreasing by 33.37%, 37.95% and 35.76% respectively. This confirms the synergistic effect between the components in the composition, indicating that only a complete combination of ingredients can exert the best melanin synthesis inhibition effect.
[0120] 3. Stability test
[0121] 1) Test samples: Examples 1-3, Comparative Examples 1-6 and Blank Example 1 described in Table 2.
[0122] 2) Test method: Internal control standard, observe the appearance color, viscosity and pH for three months.
[0123] Table 7 Stability test results
[0124] time 45℃ 40℃ 37℃ 25℃ 5℃ -15℃ CYCLE illumination 1W √ √ √ √ √ √ √ √ 2W √ √ √ √ √ √ √ √ 3W √ √ √ √ √ √ √ √ 4W √ √ √ √ √ √ √ √ 2M √ √ √ √ √ √ √ √ 3M √ √ √ √ √ √ √ √
[0125] Among them, "CYCLE" refers to the cycle, and the cycle setting is: heating from -15℃ to 45℃, and cooling from 45℃ to -15℃ for five times.
[0126] Test results: The results in Table 7 show that the essences in Examples 1-3, Comparative Examples 1-6 and Blank Example 1 were stable in properties within 3 months.
[0127] 4. Human efficacy testing
[0128] (1) Test samples: the essences of Examples 1-3, Comparative Examples 1-6 and Blank Example 1 as described in Table 2.
[0129] (2) Test subjects: 100 healthy women (aged 30-60 years) were randomly divided into 10 groups, each with 10 participants. Each group used the same formula product. Written informed consent was signed. Before enrollment, a series of questions regarding medical history and health status were asked based on the inclusion and exclusion criteria. The skin of the test site was evaluated for compliance and skin color was screened, and the results were recorded.
[0130] Environmental Conditions: During the test, visual assessment and instrument testing are conducted in an environment with a temperature of 21±1°C and a relative humidity of 50±10%. Visual assessment is conducted under constant lighting conditions (fluorescent lamps or LED lighting with a color temperature of 5500-6500K). Subjects need to acclimate to these environmental conditions for at least 30 minutes before assessment and testing.
[0131] (3) Test Method: Use the sample twice daily, morning and evening, for 4 weeks. Apply an appropriate amount of the test sample to one cheek and leave the other cheek unused. Apply sunscreen to the entire face every morning.
[0132] The test results were collected at the following three time periods: before using the sample (D0), 2 weeks after using the sample (W2), and 4 weeks after using the sample (W4).
[0133] (4) The test results can be calculated using the following formula:
[0134] Change rate = (analysis value after using the product - analysis value before using the product) ÷ analysis value before using the product × 100%
[0135] 1) Cheek skin glossiness test
[0136] The Glossymeter GL200 was used to measure cheek skin glossiness, and the results are shown in Table 8. A larger analysis value and a larger rate of change indicate an improvement in skin glossiness.
[0137] Table 8 Change rate of cheek skin glossiness
[0138] sample Use for two weeks% Use for four weeks% Example 1 10.11 20.54 Example 2 11.23 22.31 Example 3 9.45 18.85 Comparative Example 1 7.33 14.21 Comparative Example 2 7.85 14.94 Comparative Example 3 7.06 13.87 Comparative Example 4 5.41 10.31 Comparative Example 5 4.93 9.88 Comparative Example 6 5.12 10.27 Blank example 1 3.36 7.11
[0139] As shown in Table 8, after using the essence, the rate of change in skin glossiness increased with increasing usage time for both Examples 1-3 and Comparative Examples 1-6, indicating improved skin glossiness. However, compared to Comparative Examples 1-6, the rate of change in skin glossiness for Example 1-3 increased more significantly over the same usage time, indicating that the essence of Examples 1-3 significantly improved skin glossiness.
[0140] Comparison of the results of Examples 1-3 and Comparative Examples 1-6 shows that compared to the blank examples (not using the composition for achieving resistance to blue light damage through multi-pathway synergy) or using only one or two of siRNA liposomes, resveratrol, and α-arbutin (Comparative Examples 1-6), the simultaneous use of siRNA liposomes, resveratrol, and α-arbutin resulted in a greater improvement in skin gloss. This indicates that siRNA liposomes, resveratrol, and α-arbutin have a synergistic effect, effectively slowing skin aging and protecting against blue light damage.
[0141] 2) Skin texture test
[0142] Antera 3D was used to conduct skin texture testing, and the results are shown in Table 9. A smaller analysis value and a smaller rate of change indicate that skin roughness has improved.
[0143] Table 9 Skin texture change rate
[0144] sample Use for two weeks% Use for four weeks% Example 1 -9.13 -17.82 Example 2 -9.77 -18.35 Example 3 -8.62 -17.01 Comparative Example 1 -7.11 -14.32 Comparative Example 2 -7.23 -14.84 Comparative Example 3 -6.96 -14.11 Comparative Example 4 -5.52 -11.28 Comparative Example 5 -5.08 -10.29 Comparative Example 6 -5.27 -10.75 Blank example 1 -3.12 -6.03
[0145] Figure 1 The skin texture before and after using the essence of Example 3, where A is the skin texture before using the essence of Example 3, B is the skin texture after using the essence of Example 3 for two weeks, and C is the skin texture after using the essence of Example 3 for four weeks.
[0146] From Table 9 and Figure 1 As can be seen, after using the essence, the skin texture change rate of Examples 1-3 and Comparative Examples 1-6 decreased with increasing usage time, indicating that skin texture improved. However, compared to Comparative Examples 1-6, the skin texture change rate of Examples 1-3 decreased more significantly over the same usage time, indicating that the skin texture improvement effect of the essence of Examples 1-3 was more significant.
[0147] Comparison of the results of Examples 1-3 and Comparative Examples 1-6 demonstrates that the combined use of siRNA liposomes, resveratrol, and α-arbutin significantly improved skin texture compared to the use of a multi-pathway synergistic composition or the use of only one or two of siRNA liposomes, resveratrol, and α-arbutin. This demonstrates that siRNA liposomes, resveratrol, and α-arbutin synergistically improve skin texture, effectively slowing skin aging and protecting against blue light damage.
[0148] The above-described embodiments merely illustrate several implementations of the present invention, and while their descriptions are relatively specific and detailed, they should not be construed as limiting the scope of the present invention. It should be noted that a person skilled in the art would be able to make numerous variations and improvements without departing from the spirit of the present invention, all of which fall within the scope of protection of the present invention. Therefore, the scope of protection of the present invention shall be determined by the appended claims.
Claims
1. A multi-pathway synergistic anti-blue light targeted repair composition, characterized in that: The composition comprises siRNA liposome, resveratrol and alpha-arbutin in a mass ratio of (0.01-5):(0.01-5):(0.01-3).
2. The multi-pathway synergistic anti-blue light targeted repair composition according to claim 1, characterized in that: The mass ratio of the siRNA liposome, resveratrol and α-arbutin is (3-5): (1-5): (1-3).
3. The multi-pathway synergistic anti-blue light targeted repair composition according to claim 1, characterized in that: The preparation method of the siRNA liposomes: (1) Dissolve the phospholipids fully in ethanol. After the phospholipids are fully dissolved, evaporate the ethanol at low temperature to form a uniform phospholipid film. (2) Stir and mix the phosphate buffer solution and siRNA; (3) adding the mixed solution obtained in step (2) to the phospholipid membrane in step 1), performing water treatment on the phospholipid membrane, and performing ultrasonic treatment after the phospholipid membrane is completely detached to obtain functional liposomes.
4. The multi-pathway synergistic anti-blue light targeted repair composition according to claim 3, characterized in that: The mass volume ratio of phospholipid to ethanol in step (1) is (1-5): (5-50) mg / mL.
5. The multi-pathway synergistic anti-blue light targeted repair composition according to claim 3, characterized in that: The mass volume ratio of siRNA to phosphate buffer solution in step (2) is (100-500): (20-50) mg / mL.
6. A skin care product, characterized in that: The invention comprises matrix auxiliary materials and functional components, wherein the functional components include the composition according to any one of claims 1 to 5, and the weight percentage of the composition in the skin care product is 0.03-13%.
7. The skin care product according to claim 6, characterized in that The matrix excipients include phase A excipients, phase B excipients, phase C excipients and phase D excipients; Taking the weight parts of the skin care product as 100 parts, The phase A auxiliary material includes 0.05-5 parts of a thickener, 0.11-3 parts of a skin conditioner, and 3.6-10 parts of a moisturizer; The phase B auxiliary material includes 0.4-4 parts of a softener and 0.6-3 parts of an emulsifier; The phase C auxiliary material includes 0.1 to 3 parts of a pH regulator; The phase D auxiliary material includes 0.1 to 2 parts of fragrance and 0.02 to 2 parts of preservative.
8. The skin care product according to claim 7, characterized in that The thickener includes one or more of cetyl ethylhexanoate, xanthan gum, acrylates / stearyl alcohol polyether-20 methacrylate copolymer, acrylates / C10-30 alkyl acrylate crosspolymer, tamarindus indica seed polysaccharide, sodium acrylate / sodium acryloyldimethyl taurate copolymer, octyldodecanol, cetearyl dimethicone / vinyl dimethicone crosspolymer and acrylamide / sodium acryloyldimethyl taurate copolymer; The skin conditioning agent includes one or more of sodium hyaluronate, hydrolyzed sodium hyaluronate, allantoin, niacinamide, tocopheryl acetate, bisabolol, shea butter (BUTYROSPERMUM PARKII) and lavender oil (LAVANDULA ANGUSTIFOLIA); The moisturizing agent includes one or more of glycerin, propylene glycol, butylene glycol, panthenol, inositol, hyaluronic acid, β-glucan, glucose, hydrogenated lecithin, mannitol and erythritol; The emollient comprises one or more of dimethicone, caprylic / capric triglyceride, phytosteryl / octyldodecanol lauroyl glutamate, glyceryl stearate, cyclopentasiloxane, ethylhexyl palmitate, squalane, trehalose, mineral oil, glyceryl caprylate, soybean (Glycine Max) oil, jojoba (SIMMONDSIA CHINENSIS) seed oil, raspberry (RUBUSIDAEUS) seed oil, caprylyl glycol, isononyl isononanoate, isohexadecane, white meadowfoam (LIMNANTHES ALBA) seed oil, dimethiconol and olive (OLEA EUROPAEA) fruit oil; The emulsifier includes one or more of cetearyl alcohol, glyceryl stearate, PEG-30 hydrogenated castor oil, PEG-40 hydrogenated castor oil, PEG-100 stearate, cetearyl glucoside, polysorbate-20, polysorbate-80, polysorbate-60, ethylene glycol distearate, sorbitan stearate, sorbitan isostearate, sorbitan oleate, polyglyceryl-2 triisostearate and PEG-150 distearate; The pH regulator includes one or more of citric acid, sodium citrate, arginine and lactic acid; The aromatic agent includes essence; The preservatives include one or more of methylparaben, propylparaben, phenoxyethanol, ethylhexylglycerin and pentylene glycol.
9. The method for preparing the skin care product according to claim 7, wherein: The steps include: a. Aqueous phase: After fully moistening and mixing the components of phase A excipients, add them to water, stir thoroughly until completely dissolved, and heat; b. Oil phase; mix and heat the B phase excipients, stirring until completely dissolved; c. Emulsification: Add the mixture from step b to the aqueous phase from step a, stirring and homogenizing; d. Add phase C auxiliary material, stir and homogenize, and cool to 40-50℃; e. Add phase D auxiliary material and stir; f. After stirring and cooling to 35-38 ° C, add the effective ingredient composition E, stir and homogenize to obtain the product.
10. The method for preparing the skin care product according to claim 9, characterized in that: The heating temperature in steps a to b is 75 to 85° C. The stirring speed in steps c to f is 200 to 400 rpm, and the stirring time is 3 to 10 minutes; The homogenization speed in steps c to f is 2000 to 4000 rpm, and the homogenization time is 3 to 5 minutes.
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