Application of ascorbyl glucoside in health food and oral care product

Abstract

The invention provides application of ascorbyl glucoside in health food and oral care products, and belongs to the field of health food and oral care, and the configuration of the ascorbyl glucoside is 2-O-alpha-D-glucosyl-L-ascorbic acid (AA2G). The AA2G can be used for effectively inhibiting the activity of alpha-glucosidase and has a relatively high binding rate to bile acid; animal experiments show that AA2G can significantly reduce the blood sugar concentration, serum triglyceride (TG) concentration and serum total cholesterol (TC) concentration of diabetic model mice, and has the efficacy of assisting in reducing blood sugar and blood fat. In addition, the AA2G also has an inhibiting effect on streptococcus mutans and porphyromonas gingivalis, and has a decayed tooth resisting effect. In addition, the AA2G can continuously and stably exert the effect of assisting in reducing blood sugar, and the long-acting blood sugar reducing capacity of the AA2G is obviously superior to that of VC and beta-configuration ascorbic acid glucoside (AA-2beta G). The AA2G is applied to health-care food and oral care products, and can effectively reduce blood sugar and blood fat and effectively improve the problem of decayed teeth.

Description

Technical Field

[0001] The present invention relates to the fields of health foods and oral care, and particularly relates to the application of ascorbyl glucoside in health foods for assisting in reducing blood sugar and blood lipid and in oral care products. Background Art

[0002] With the improvement of people's living standards, high-sugar foods such as milk tea, carbonated drinks, and baked desserts are loved by many people because of their delicious taste. However, excessive intake of sugar will have an adverse impact on health. High-sugar and high-fat foods and beverages have high calories, and excessive intake is likely to cause fat accumulation and thus lead to obesity. Long-term unhealthy eating habits burden the body and are prone to symptoms of high blood sugar and high blood lipid. In addition, the carbohydrates remaining in the oral cavity are easily fermented by the oral floating bacteria - Streptococcus mutans that are early colonized on the tooth surface to produce acid, and can form an adhesive plaque on the tooth surface, making the organic acids produced contact the tooth surface for a long time, causing damage to the hard tissue of the teeth, forming dental caries, and affecting oral health. Porphyromonas gingivalis is a late colonizing bacterium and plays a leading role in periodontal disease. At present, the main treatment for bacterial infectious oral problems at home and abroad is the chemotherapy of oral antibiotics. However, long-term use of antibiotics will disrupt the balance of the oral ecosystem and also exacerbate bacterial drug resistance.

[0003] The common health foods for assisting in reducing blood sugar and blood lipid on the market mainly involve natural products and vitamins. Among them, vitamin C, as a multi-functional raw material that can be both eaten and used in cosmetics, is widely used. Vitamin C (also known as ascorbic acid, VC) is a vitamin that participates in various physiological activities of the human body. Since the hydroxyl group on C2 is easily affected by pH, metal ions, heat, and light, the stability of VC is poor. Therefore, various relatively stable derivatives, such as salts, esters, and glycosyl derivatives, have been developed successively.

[0004] 2-O-α-D-glucosyl-L-ascorbic acid in ascorbyl glucoside, also known as AA2G. AA2G is synthesized by chemically and biologically modifying the C-2 of the ascorbic acid molecule. The hydroxyl group of the 2,3-enediol of the ascorbic acid molecule is replaced by a glucosyl group linked by an α-1,4-glycosidic bond. This hydroxyl group is the unstable and antioxidant site of ascorbic acid, and the introduced glucosyl group plays a masking role. Therefore, AA2G has good stability and antioxidant properties. Specifically, (1) AA2G has strong stability, can resist adverse conditions such as light, oxygen, and heavy metals, and it can be absorbed by the human body and slowly hydrolyzed and released in the human body to continuously supplement human ascorbic acid. Therefore, it can be used as a stabilizer, ascorbic acid supplement, etc. in food to improve food quality. (2) AA2G has the effects of promoting collagen synthesis, inhibiting melanin formation, and absorbing and resisting ultraviolet rays, making the skin firm and elastic, whitening, and preventing photoaging. Due to its good collagenolytic activity and easy absorption by the skin, it is widely used in the cosmetics industry. (3) In animal husbandry, AA2G can promote the growth and development of animals, promote egg production in breeding hens, improve the lactation ability of sows and the sperm motility of breeding boars, and improve the health status of animals. (4) In the medical field, the antioxidant effect of AA2G is beneficial to improving human immunity, inhibiting viral and bacterial infections, treating infections after injury and surgery, and preventing and treating colds, etc.

[0005] In summary, AA2G has strong stability and plays an important role in aspects such as whitening, anti-wrinkle, firming, and improving immunity. However, there is currently no research on its application in assisting blood sugar lowering, lipid lowering, and oral care. Summary of the Invention

[0006] In view of the existing research gap, the present invention aims to provide an application of ascorbyl glucoside in health foods and oral care products.

[0007] The technical solution adopted by the present invention is as follows:

[0008] In the first aspect of the present invention, there is provided an application of ascorbyl glucoside in the preparation of a health food for lowering blood sugar and / or blood lipid, wherein the ascorbyl glucoside is 2-O-α-D-glucosyl-L-ascorbic acid.

[0009] Optionally, the health food includes beverages, oral liquids, tablets, granules, jelly gels, capsules, or syrups.

[0010] In the second aspect of the present invention, there is provided a health food for lowering blood sugar and / or blood lipid, which includes ascorbyl glucoside, wherein the ascorbyl glucoside is 2-O-α-D-glucosyl-L-ascorbic acid.

[0011] Optionally, the health food further comprises excipients acceptable in the health food.

[0012] In a third aspect of the present invention, there is provided an application of glucosylascorbic acid in the preparation of an oral care product for anti-caries, wherein the glucosylascorbic acid is 2-O-α-D-glucosyl-L-ascorbic acid.

[0013] Optionally, the oral care product includes toothpaste, tooth powder, oral spray or mouthwash.

[0014] In a fourth aspect of the present invention, there is provided an oral care product for anti-caries, which includes glucosylascorbic acid, and the glucosylascorbic acid is 2-O-α-D-glucosyl-L-ascorbic acid.

[0015] Optionally, the oral care product further comprises excipients acceptable in the oral care product.

[0016] Beneficial effects: The present invention provides an application of glucosylascorbic acid in health foods and oral care products. The configuration of the glucosylascorbic acid is 2-O-α-D-glucosyl-L-ascorbic acid (AA2G). The AA2G can effectively inhibit the activity of α-glucosidase and has a high binding rate to bile acids. From animal experiments, it can be seen that AA2G can significantly reduce the blood glucose concentration, serum triglyceride (TG) concentration, and serum total cholesterol (TC) concentration of diabetic model mice, and has the effects of assisting in reducing blood sugar and blood lipids. In addition, AA2G also has an inhibitory effect on Streptococcus mutans and Porphyromonas gingivalis, and has an anti-caries effect. Furthermore, AA2G can continuously and stably exert the effect of assisting in reducing blood sugar, and its long-term blood sugar-lowering ability is significantly better than that of VC and β-configured glucosylascorbic acid (AA-2βG). When the AA2G is applied to health foods and oral care products, it can effectively reduce blood sugar and blood lipids and effectively improve dental caries problems. Description of the Drawings

[0017] Figure 1 It is a graph showing the inhibition rate of AA2G on α-glucosidase in Example 1 of the present invention.

[0018] Figure 2 It is a graph showing the bile acid binding rate of AA2G in Example 2 of the present invention.

[0019] Figure 3 It is a graph showing the effect of AA2G on the blood glucose concentration of mice in Example 3 of the present invention.

[0020] Figure 4 It is a graph showing the effect of AA2G on the serum triglyceride (TG) of mice in Example 3 of the present invention.

[0021] Figure 5This is the effect diagram of AA2G on total cholesterol (TC) in mouse serum in Example 3 of the present invention.

[0022] Figure 6 This is the effect comparison diagram of AA2G, AA-2βG and VC on blood glucose concentration at different time points in Example 4 of the present invention.

[0023] Figure 7 This is the effect comparison diagram of AA2G, AA-2βG and VC on serum VC concentration at different time points in Example 4 of the present invention.

[0024] Figure 8 This is the effect comparison diagram of AA2G, AA-2βG and VC on blood glucose concentration 45 days after administration in Example 4 of the present invention. Detailed implementation manners

[0025] The present invention provides an application of ascorbyl glucoside in health foods and oral care products. To make the objectives, technical solutions and effects of the present invention clearer and more definite, the present invention is further described in detail below. The specific embodiments described herein are only used to explain the present invention, and the protection scope is not limited to the content described.

[0026] Ascorbyl glucoside can be divided into α-configuration and β-configuration according to different configurations. The configuration involved in the present invention is 2-O-α-D-glucosyl-L-ascorbic acid (abbreviated as AA2G), and its chemical structural formula is:

[0027]

[0028] The present invention provides the application of AA2G in health foods and oral care, especially in aspects of assisting in reducing blood sugar, reducing blood lipid and anti-caries.

[0029] When the AA2G described in the present invention is used for health foods, it can exist in the forms of beverages, oral liquids, tablets, granules, jelly gels, capsules, syrups, but not limited thereto.

[0030] When the AA2G described in the present invention is used for oral care products, it can exist in the forms of toothpaste, tooth powder, oral spray or mouthwash, but not limited thereto.

[0031] In other words, the health foods and oral care products described in the present invention are not limited to the above several forms. Any products containing AA2G and used for assisting in reducing blood sugar, reducing blood lipid and anti-caries should fall within the protection scope of the present invention.

[0032] The present invention is described in detail below through specific embodiments.

[0033] Example 1

[0034] Detection of α-Glucosidase Inhibitory Activity

[0035] α-Glucosidase inhibitors are an important class of drugs for the alleviation and treatment of non-insulin-dependent diabetes. Therefore, the inhibitory rate of α-glucosidase is used to evaluate the hypoglycemic ability of samples. The experimental design is shown in Table 1, and the calculation formula for the inhibitory rate of α-glucosidase is shown in (1):

[0036] Inhibitory rate of α-glucosidase = 1 - (A1 - A2) / (A3 - A4) * 100%.............(1)

[0037] Table 1. Experimental design table for α-glucosidase

[0038]

[0039] The results are shown in Table 2 below, and its inhibitory rate curve is as Figure 1 shown:

[0040] Table 2. Inhibitory rate of samples on α-glucosidase

[0041]

[0042]

[0043] As shown in Table 2, when AA2G is at 4 - 40 mg / mL, with the increase of the sample concentration, the inhibitory rate of the sample on α-glucosidase gradually increases, which are 6.92%, 15.36%, 18.25%, 31.42%, 47.06%, and 96.38% respectively, and the P values are all less than 0.05. This indicates that AA2G exhibits excellent hypoglycemic ability.

[0044] Example 2

[0045] Determination of Bile Acid Binding Ability

[0046] The biosynthesis of bile acids provides an important pathway for cholesterol metabolism. The binding of bile acids can prevent their reabsorption and stimulate the conversion of cholesterol in plasma and liver into bile acids, consuming more cholesterol. Therefore, by measuring the binding ability with bile acids, the effect of the sample on reducing the body's cholesterol level is verified, thereby proving its ability to assist in reducing blood lipids.

[0047] An appropriate amount of the sample was added to 1 mL of HCl (0.01 mol / L) and digested in a 37 °C water bath for 1.5 h. This step simulated the gastric digestion process: the pH of the reaction system was adjusted to 7.0 with 0.1 mol / L NaOH aqueous solution, 5 mL of pancreatin and 4 mL of diluted bile acid solution were added, and after reacting in a 37 °C water bath for 1 h, it was centrifuged at 10000 r / min for 10 min. Then, the supernatant was taken to measure the bile acid content by a bile acid kit (TBA) (enzyme cycling method). Cholestyramine was used as the positive control group, and PBS was used to replace the sample as the blank control group.

[0048] The calculation formula for the bile acid binding rate is shown in (2):

[0049] Bile acid binding rate = (bile acid concentration in the blank control group - bile acid concentration in the sample group) / bile acid concentration in the blank control group * 100%...............(2)

[0050] The results are shown in Table 3 below, and its binding rate curve is as Figure 2 shown:

[0051] Table 3. Bile acid binding rate of the sample

[0052]

[0053] As shown in Table 3: When AA2G was at 10 - 50 mg / mL, with the increase of the sample concentration, the bile acid binding rate gradually increased, which were 8.50%, 20.19%, 43.24%, 50.18%, 68.55%, 86.25% respectively, and the P values were all less than 0.05. This indicated that AA2G had the effect of assisting in reducing blood lipid.

[0054] Example 3

[0055] Detection of the effects on blood glucose and blood lipid of experimental diabetic mice

[0056] SPF - level adult male Kunming mice (body weight 20 - 25 g) were used to establish a high - sugar and high - fat model by feeding with high - sugar and high - fat diet and intraperitoneal injection of alloxan.

[0057] (1) High - sugar and high - fat model establishment

[0058] Experimental mice were allowed free access to food and water and were adaptively fed for one week at a temperature maintained at 20 ± 2 °C and a relative humidity of 55% ± 5%. After one week, the mice were randomly divided into two groups. The blank group (≥10 mice) was fed with normal feed, and the model group (≥50 mice) was fed with a high-sugar and high-fat diet. After 8 weeks of free access to water and food for both groups, both groups were fasted but allowed water for 24 h. Then, the blank group was injected with normal saline, and the model group was intraperitoneally injected with alloxan solution at a dose of 120 mg / (kg·bw). Three days after modeling, the fasting blood glucose of the mice was measured. Mice with blood glucose higher than 20 mmol / L were considered high-sugar and high-fat model mice. Fifty mice with successful modeling were randomly divided into five groups, namely, the high-sugar and high-fat group, three sample groups (i.e., the high-dose sample group, the medium-dose sample group, and the low-dose sample group), and the positive control group, with 10 mice in each group.

[0059] (2) Observation indicators and detections

[0060] During the experiment, the blank group and the high-sugar and high-fat group were gavaged with normal saline, the three sample groups (i.e., the high-dose sample group, the medium-dose sample group, and the low-dose sample group) were gavaged with AA2G at doses of 50, 200, and 300 mg / (kg·bw), and the positive control group was gavaged with metformin (100 mg / (kg·bw)). During the experiment, the mice had free access to water. The blank group maintained a normal diet, and the remaining five groups maintained a high-sugar and high-fat diet. The experimental period was 45 days. After the last administration, the mice were fasted for 12 h, anesthetized, and blood was collected from the tail. The blood glucose was measured using a blood glucose meter, and the serum triglyceride (TG) and total cholesterol (TC) of the mice were measured using a kit.

[0061] (3) Results and analysis

[0062] As shown in Table 4:

[0063] Table 4. Effects of the sample on the blood glucose of experimental diabetic mice

[0064]

[0065] Note: *: Sample group vs. high-sugar and high-fat group (NC), P < 0.05; Δ: M group vs. blank group (BC), P < 0.05

[0066] A high-sugar and high-fat mouse model was constructed by using a high-sugar and high-fat diet and intraperitoneal injection of alloxan. AA2G was used to gavage the mice in the modeling group. The results are shown in Table 4. The differences in different indicators among the four groups are as Figure 3 、 Figure 4 、 Figure 5As shown: Compared with the blank group (BC), the concentrations of three indicators, namely blood glucose, serum triglyceride (TG), and serum total cholesterol (TC), in the high-sugar and high-fat group (M) increased, showing significant differences, indicating successful model establishment; the PC group was significantly lower than the M group, with significant differences (P<0.05), indicating the effectiveness of the experiment; the concentrations of the three indicators in the sample group were significantly lower than those in the M group, with significant differences (P<0.05). The blood glucose, TG, and TC in the sample group showed significant decreases compared with the M group, indicating that AA2G has the effect of assisting in reducing blood glucose and blood lipids.

[0067] Example 4

[0068] Comparison of the biological activities of AA2G, AA-2βG, and VC in reducing blood glucose

[0069] Experimental diabetic mice with the same treatment method as in Example 3 were used, and a blank group (number of mice ≥ 10), a high-sugar and high-fat group (number of mice ≥ 10), a positive control group (number of mice ≥ 10), and a sample group (number of mice ≥ 10) were set up. The feeding methods of the mice in each group were the same as in Example 3. The sample group consisted of three groups, namely VC at 55 mg / (kg·bw), AA2G at 105 mg / (kg·bw), and AA-2βG at 105 mg / (kg·bw), and the test period was 45 days. 30 minutes after the first administration, blood was drawn to detect the VC content and blood glucose content in the three sample groups, and no feed was given within the subsequent 8 hours. Subsequently, blood was drawn at 2 h, 3 h, 5 h, and 8 h to detect the VC and blood glucose contents in the serum of each group. The positive control group was metformin at 100 mg / (kg·bw). The blank group, the high-sugar and high-fat group, and the positive control group collected blood at the same time points as the sample group, and only the blood samples at the 8th hour were detected and analyzed; after fasting for 12 hours after the last administration, blood was collected from the tail after anesthesia, and a blood glucose meter was used to measure its blood glucose.

[0070] The results of the change in blood glucose concentration over time are shown in Table 5, and the change curve of blood glucose concentration over time is as Figure 6 shown:

[0071] Table 5. Comparison of blood glucose concentrations of AA2G, AA-2βG, and VC at different time points

[0072]

[0073]

[0074] Note: There are significant differences when P<0.05, and there are no significant differences when P≥0.05.

[0075] The results of the change in VC concentration in the serum over time are shown in Table 6, and the change curve of VC concentration over time is as Figure 7 shown:

[0076] Table 6. Comparison of VC concentrations in serum of AA2G, AA-2βG and VC at different time points

[0077]

[0078] Note: There is a significant difference when P < 0.05, and there is no significant difference when P ≥ 0.05.

[0079] The mice after modeling were used as the research objects. Blood glucose concentration was detected at 0.5, 2, 3, 5, and 8 h after the first administration to compare the blood glucose-lowering ability among the sample groups.

[0080] As time increased, from 0.5 to 2 h, the blood glucose concentration in the VC group decreased significantly. From 3 to 8 h, VC lost its ability to control blood glucose, and the blood glucose concentration was close to that of the M group. At 0.5 h, the blood glucose concentration level in the AA2G group was comparable to that in the VC group and the AA-2βG group (P > 0.05). From 2 to 8 h, the blood glucose concentration in the AA2G group was lower than that in the VC group and the AA-2βG group, and the difference was significant. At each time point, the blood glucose concentration in the AA2G group was lower than that in the AA-2βG group (P < 0.05), indicating that the blood glucose-lowering effect was AA2G group > AA-2βG group > VC group.

[0081] The VC concentration in the serum of each group also fluctuated greatly with time. At 0.5 h, the VC concentrations in the serum of the AA-2βG group and the VC group were the highest among the three groups. At 2 h, the VC concentration in the serum of the AA2G group was the highest. This shows that AA2G takes longer to decompose into VC in the blood than AA-2βG. From 5 to 8 h, the VC concentration in the serum of the VC group was at a relatively low level and in a numerical equilibrium state, with no significant difference from the BC and M groups; the VC concentrations in the serum of the AA2G group and the AA-2βG group reached the highest value at 5 h, and the VC concentration in the serum of the AA2G group was higher than that in the AA-2βG group, and reached the lowest at 8 h. In a short time, VC had a better effect on rapidly lowering blood glucose, while AA2G and AA-2βG had a better effect on lowering blood glucose and maintaining stability. Comprehensive evaluation showed that the blood glucose-lowering effect was in the order of AA2G group > AA-2βG group > VC group.

[0082] Bioactivity comparison after the first administration: The above data indicate that VC rapidly enters the body and exerts its hypoglycemic effect at 0.5 h. Due to the relatively stable structures of AA2G and AA-2βG, they cannot be rapidly decomposed by glucosidase in the body to release VC and exert the hypoglycemic effect. As time increases, VC is gradually decomposed due to its active chemical properties, leading to an increase in blood glucose and a decrease in the VC concentration in serum. However, AA2G and AA-2βG are gradually decomposed into VC, so the VC concentration in these two groups of sera increases and the blood glucose concentration gradually decreases. The unstable nature of VC results in its inability to exert a long-term effect in the body. AA2G can decompose into VC more efficiently and stably over a long period compared to AA-2βG and effectively reduce the blood glucose concentration. Therefore, AA2G has higher bioactivity in assisting hypoglycemia compared to VC and AA-2βG. Within 8 h after administration, the onset duration is AA2G > AA-2βG > VC.

[0083] The effects on blood glucose concentration after 45 days of administration are shown in Table 7, Figure 8 as follows:

[0084] Table 7. Comparison of blood glucose concentrations of AA2G, AA-2βG, and VC after 45 days of administration

[0085]

[0086] Note: There is a significant difference when P < 0.05, and there is no significant difference when P ≥ 0.05.

[0087] After 45 days of administration, the blood glucose concentration in the AA2G group is lower than that in the VC group and the AA-2βG group. Combining the results of the first administration, it can be shown that AA2G continuously and stably exerts its hypoglycemic effect within 8 h, and its long-term hypoglycemic ability is significantly better than that of VC and AA-2βG. AA2G can be used in health foods for rapid hypoglycemia.

[0088] Example 5

[0089] Evaluation method for the minimum inhibitory concentration (MIC):

[0090] Take 10.0 mL of sample solutions at different dilution degrees and add them to a petri dish. Then add 10 mL of double-strength solid agar medium (in a 45 °C water bath) to the petri dish, and shake the petri dish while adding to ensure that the sample solution and the medium are fully mixed. After solidification, it is ready for use. The media required for Streptococcus mutans and Porphyromonas gingivalis are double-strength TSA + 10% defatted sheep blood medium.

[0091] Set up two parallels in the experiment. Use a pipette to take 1 - 2 μL of the bacterial suspension (with a bacterial content of about 10 7Seed (CFU / mL) into a petri dish containing the test sample solution medium. The diameter of the bacterial solution circle formed after inoculation is about 5 mm to 8 mm. Inoculate the bacterial solution into an agar plate without the test sample solution in the same way as a positive control; in the same way, a test tube without inoculating the bacterial solution is used as a negative control, and place it in an anaerobic incubator at 37°C for 24 h to 48 h for observation. The lowest antibacterial (inhibitory) solution concentration at which colony growth is completely inhibited is the MIC of the sample against the test bacteria.

[0092] The results are shown in Tables 8 and 9 as follows:

[0093] Table 8. Antibacterial (MIC) test results of AA2G against Streptococcus mutans

[0094]

[0095] Note: "+" indicates "turbid with bacteria"; "-" indicates "transparent and bacteria-free"

[0096] Table 9. Antibacterial (MIC) test results of AA2G against Porphyromonas gingivalis

[0097]

[0098] Note: "+" indicates "turbid with bacteria"; "-" indicates "transparent and bacteria-free"

[0099] The negative control was in a transparent state and the positive control was in a turbid state, indicating that this experiment was valid. The MICs of AA2G against Streptococcus mutans and Porphyromonas gingivalis were 1.0% and 2.0% respectively, indicating that AA2G had an inhibitory effect on Streptococcus mutans and Porphyromonas gingivalis.

[0100] Example 6

[0101] Take a standard qualitative filter paper with a diameter of 5 mm, sterilize it by high-pressure steam and dry it, and then store it for later use. In a laminar flow hood, use a sterilized pipette tip to aspirate a bacterial solution with a concentration of 10 5 ~10 6 CFU / mL, and spread it evenly on the plate to prepare plates of two bacteria (Streptococcus mutans and Porphyromonas gingivalis) respectively, and leave it to dry at room temperature for 5 min. Take 4 sterilized filter papers and place them at the center of the plate respectively, and mark the positions. Drop 20 μL of AA2G solution onto 3 of the filter papers, and drop sterilized normal saline onto the other filter paper as a negative control group. Prepare another plate as a positive control group, using metronidazole solution, and the operation steps are the same as those of the test sample. Invert the plate, place it in an anaerobic incubator at 37°C for 24 h to 48 h for observation, and measure the diameter of the inhibition zone. Result determination: If the diameter of the inhibition zone is greater than 7 mm, it is judged to have an antibacterial effect; if the diameter of the inhibition zone is less than or equal to 7 mm, it is judged to have no antibacterial effect.

[0102] The results are shown in Table 10 and Table 11 as follows:

[0103] Table 10. Antibacterial (inhibition zone) test results of AA2G against Streptococcus mutans

[0104]

[0105] Table 11. Antibacterial (inhibition zone) test results of AA2G against Porphyromonas gingivalis

[0106]

[0107]

[0108] The antibacterial zone test results of AA2G against Streptococcus mutans are shown in Table 10. The diameters of the inhibition zones in the negative control group were all less than 7 mm, and those in the positive control group were all greater than 7 mm, indicating that this experiment was valid. When AA2G was at 5% - 15%, as the sample concentration increased, the average diameter of the inhibition zone gradually increased, being 7, 7.90, 8.29, 9.11, 9.72 mm respectively. When AA2G was in the concentration range of 7.5% - 15%, the diameters of the inhibition zones were all greater than 7 mm, and AA2G showed an inhibitory effect on Streptococcus mutans within this concentration range.

[0109] The antibacterial zone test results of AA2G against Porphyromonas gingivalis are shown in Table 11. The diameters of the inhibition zones in the negative control group were all less than 7 mm, and those in the positive control group were all greater than 7 mm, indicating that this experiment was valid. When AA2G was at 6% - 12%, as the sample concentration increased, the average diameter of the inhibition zone gradually increased, being 8.43, 9.83, 11.66, 11.67 mm respectively, and the diameters of the inhibition zones were all greater than 7 mm, indicating that AA2G showed an inhibitory effect on Porphyromonas gingivalis within this concentration range.

[0110] In summary, the present invention provides an application of ascorbyl glucoside in products for assisting in reducing blood sugar, lipid-lowering and anti-caries. The specific configuration involved in the present invention is 2-O-α-D-glucosyl-L-ascorbic acid (abbreviated as AA2G). The AA2G can effectively inhibit the activity of α-glucosidase and has a high binding rate to bile acids. From the animal experiments, it can be seen that AA2G can significantly reduce the blood sugar concentration, serum triglyceride (TG) concentration, and serum total cholesterol (TC) concentration of diabetic model mice, and has the effects of assisting in reducing blood sugar and lipid-lowering. In addition, AA2G can also significantly inhibit Streptococcus mutans and Porphyromonas gingivalis, and has an anti-caries effect. Furthermore, regarding the sustainable and stable exertion of the blood sugar-lowering effect of AA2G, its long-term blood sugar-lowering ability is significantly better than that of VC and AA-2βG. The AA2G is applied in health foods and oral care products, which can effectively reduce blood sugar and lipids and improve dental caries problems.

[0111] The above embodiments are only used to illustrate the technical solutions of the present invention, rather than to limit it; although the present invention has been described in detail with reference to the foregoing embodiments, for those of ordinary skill in the art, it is still possible to modify the technical solutions described in the foregoing embodiments, or perform equivalent replacements on some of the technical features, and these modifications or replacements do not cause the essence of the corresponding technical solutions to deviate from the spirit and scope of the technical solutions claimed by the present invention.

Claims

1. Use of glucosyl ascorbate in the preparation of a health food for lowering blood glucose and / or blood lipid, wherein the glucosyl ascorbate is 2-O-α-D-glucosyl-L-ascorbic acid.

2. The application according to claim 1, wherein The health food includes beverages, oral liquids, tablets, instant granules, jelly gels, capsules or syrups.

3. A health food for reducing blood sugar and / or blood lipid, characterized in that, It includes glucosyl ascorbate, wherein the glucosyl ascorbate is 2-O-α-D-glucosyl-L-ascorbic acid.

4. The health food according to claim 3, characterized in that, The health food further includes excipients acceptable in the health food.

5. Use of glucosyl ascorbate in the preparation of an oral care product for anti-caries, wherein the glucosyl ascorbate is 2-O-α-D-glucosyl-L-ascorbic acid.

6. The application according to claim 5, characterized in that, The oral care product includes toothpaste, tooth powder, oral spray or mouthwash.

7. An oral care product for anti-caries, characterized in that, It includes glucosyl ascorbate, wherein the glucosyl ascorbate is 2-O-α-D-glucosyl-L-ascorbic acid.

8. The oral care product for anti-caries according to claim 7, characterized in that, The oral care product further includes excipients acceptable in the oral care product.

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