Use of a plant starch in the preparation of a product for protecting the liver from alcohol
By using golden taro starch in hangover-detoxifying products to increase the activity of enzymes in the ethanol metabolic pathway, the problem of large side effects of existing treatments for acute alcoholic liver damage is solved, effective hangover-detoxifying and liver-protecting effects are achieved, and liver health is significantly improved.
Patent Information
- Application Number
- CN202411971884.5
- Authority / Receiving Office
- CN · China
- Patent Type
- Patents(China)
- Current Assignee / Owner
- Filing Date
- 2024-12-30
- Publication Date
- 2025-10-10
- Estimated Expiration
- 2044-12-30
AI Technical Summary
Existing methods for treating acute alcoholic liver injury have side effects. It is of great significance to explore bioactive substances with hepatoprotective effects from natural resources to alleviate alcoholic liver injury.
By using golden taro starch in the preparation of hangover-relieving products, the metabolism of ethanol and acetaldehyde is accelerated, the activity of alcohol dehydrogenase and acetaldehyde dehydrogenase is increased, the levels of alanine aminotransferase and aspartate aminotransferase in serum are reduced, the activity of antioxidant enzymes is increased, and the abnormal lipid accumulation induced by ethanol is improved, thereby preparing products for preventing and/or treating liver damage caused by drinking.
Golden taro starch can speed up the time of drunkenness, reduce the drunkenness rate, significantly reduce the levels of ALT, AST, TC, TG and LDL-C in serum, increase the activity of CAT, SOD, GSH and GSH-Px, reduce MDA content, improve liver fat accumulation, and provide an effective solution for alcohol detoxification and liver protection.
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Abstract
Description
Technical Field
[0001] The invention belongs to the field of biotechnology, and particularly relates to application of plant starch in preparing a product for sobering up and protecting the liver. Background Art
[0002] Acute alcoholic liver injury (ALI) refers to severe pathological changes in the liver caused by heavy drinking over a short period of time. Clinical manifestations include abnormal liver function and liver histological changes. In recent years, the incidence of ALI caused by excessive alcohol consumption has increased significantly. ALI can lead to liver diseases such as hepatitis, fatty liver disease, and cirrhosis. After alcohol enters the body, 90% is metabolized by the liver, primarily through the oxidative pathway involving alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).
[0003] Modern treatments for alcohol-induced acute liver injury primarily rely on interventions such as corticosteroids, S-adenosylmethionine, pentoxifylline, specific anti-tumor necrosis factor α (TNF-α) antibody therapy, antioxidants, and restoration of intestinal function. Silymarin, a commonly used clinical medication for liver injury, has significant side effects, such as nausea, vomiting, abdominal pain, loss of appetite, and diarrhea. Silymarin is excreted from the liver, and long-term use may result in an inability of the liver to fully metabolize the drug, thereby increasing the burden on the liver. Therefore, it is important to explore bioactive substances with hepatoprotective properties from natural resources to mitigate alcohol-induced liver damage. Summary of the Invention
[0004] The present invention aims to solve at least one of the technical problems existing in the above-mentioned prior art. To this end, the present invention provides an application of golden yam starch in preparing a hangover relief product.
[0005] The present invention also proposes the use of golden taro starch in preparing a product for preventing and / or treating liver damage caused by drinking.
[0006] The present invention also provides a product.
[0007] According to a first aspect of the present invention, the use of golden taro starch in preparing a hangover relief product is proposed.
[0008] According to a second aspect of the present invention, the use of golden taro starch in preparing a product for preventing and / or treating liver damage caused by drinking is proposed.
[0009] In some embodiments of the present invention, the alcohol-induced liver damage includes alcohol-induced acute liver damage.
[0010] In some embodiments of the present invention, the product has at least one of the following functions:
[0011] (1) Accelerate the metabolism of ethanol and / or acetaldehyde;
[0012] (2) Shorten the time of drunkenness and sobering up;
[0013] (3) Reduce the rate of drunkenness;
[0014] (4) Reduce liver index;
[0015] (5) Increase the activity of alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH) in the body;
[0016] (6) Reduce serum alanine aminotransferase (ALT) and / or aspartate aminotransferase (AST) levels;
[0017] (7) Increase the activities of catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-Px);
[0018] (8) Reduce malondialdehyde (MDA) content;
[0019] (9) Improve ethanol-induced abnormal lipid accumulation;
[0020] (10) Prevent alcohol metabolism disorders caused by excessive alcohol intake.
[0021] In some embodiments of the present invention, increasing the ADH and ALDH enzyme activities in the body includes increasing the ADH and ALDH enzyme activities in the liver.
[0022] In some embodiments of the present invention, the improvement of ethanol-induced abnormal lipid accumulation includes reducing the levels of triglycerides (TG), cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) in serum, and increasing the level of high-density lipoprotein cholesterol (HDL-C) in serum.
[0023] According to a third aspect of the present invention, a product for sobering up or preventing liver damage caused by drinking is provided, wherein the product comprises the above-mentioned golden taro starch.
[0024] In some embodiments of the present invention, the product further comprises a pharmaceutically acceptable excipient.
[0025] In some embodiments of the present invention, the pharmaceutically acceptable excipients include at least one of a diluent, an excipient, a filler, a binder, a disintegrant, an absorption enhancer, a surfactant, an adsorption carrier, a lubricant, a sweetener, and a flavoring agent.
[0026] In some embodiments of the invention, the excipient comprises water.
[0027] In some embodiments of the present invention, the filler comprises at least one of starch and sucrose.
[0028] In some embodiments of the present invention, the binder comprises at least one of a cellulose derivative, alginate, gelatin, and polyvinyl pyrrolidone.
[0029] In some embodiments of the invention, the humectant comprises glycerin.
[0030] In some embodiments of the present invention, the disintegrant comprises at least one of agar, calcium carbonate and sodium bicarbonate.
[0031] In some embodiments of the present invention, the absorption enhancer comprises a quaternary ammonium compound.
[0032] In some embodiments of the invention, the surfactant comprises cetyl alcohol.
[0033] In some embodiments of the present invention, the adsorption carrier includes at least one of kaolin and bentonite.
[0034] In some embodiments of the present invention, the lubricant includes at least one of talc, calcium stearate, magnesium stearate and polyethylene glycol.
[0035] In some embodiments of the present invention, the dosage form of the product is in the form of solid, semi-solid or liquid, and can be an aqueous solution, non-aqueous solution or suspension.
[0036] In some embodiments of the present invention, the dosage form of the product is tablets, capsules, soft capsules, granules, pills, oral liquids, dry suspensions, pellets, dry extracts, injections or infusions, transdermal agents, and transdermal microneedles.
[0037] In some embodiments of the present invention, the administration method of the product can be a conventional administration method in the art, including but not limited to injection or oral administration.
[0038] In some embodiments of the present invention, the injection administration can be intravenous injection, intramuscular injection, intraperitoneal injection, intradermal injection or subcutaneous injection.
[0039] In some embodiments of the present invention, the mass fraction of the golden taro starch in the product is 0.01% to 100%.
[0040] According to some preferred embodiments of the present invention, the mass fraction of the golden taro starch in the product is 0.05% to 95%.
[0041] According to some preferred embodiments of the present invention, the mass fraction of the golden taro starch in the product is 0.05% to 50%.
[0042] According to some embodiments of the present invention, at least the following beneficial effects are achieved: the present invention proposes for the first time that golden taro starch can be effectively used for alcohol detoxification and liver protection, including enhancing the activity of key enzymes ADH and ALDH in the ethanol metabolic pathway, accelerating the rate of ethanol metabolism in the body, and reducing liver damage caused by drunkenness, having a protective effect on the body. At the same time, it can reduce the drunkenness rate, shorten the drunkenness time, significantly reduce the body's ALT, AST, TC, TG and LDL-C levels, increase the HDL-C content, significantly increase the body's liver CAT, SOD, GSH and GSH-Px activities, reduce the liver's MDA content, and significantly improve the body's liver fat accumulation, providing a new direction for the preparation of alcohol detoxification and liver protection products. BRIEF DESCRIPTION OF THE DRAWINGS
[0043] The present invention will be further described below with reference to the accompanying drawings and embodiments, in which:
[0044] Figure 1 Figure 1 shows the test results of mouse weight and drunkenness rate in Example 1 of the present invention, wherein A shows the test results of mouse weight, and B shows the test results of drunkenness rate. ###p<0.001 compared with the normal group; *p<0.05, **p<0.01 compared with the model group (n=10);
[0045] Figure 2 Figures 1 and 2 show the liver phenotype and liver index test results in Example 1 of the present invention, where A shows the liver morphology and B shows the liver index test results. ####p<0.0001 compared with the normal group; *p<0.05, **p<0.01 compared with the model group (n=10).
[0046] Figure 3 Figure 1 is a graph showing the results of alcohol detoxification enzyme detection in Example 1 of the present invention, wherein A is the ADH enzyme detection result graph, and B is the ALDH enzyme detection result graph, ##p<0.01, ###p<0.001 compared with the normal group; *p<0.05, **p<0.01, ***p<0.001 compared with the model group, (n=10));
[0047] Figure 4Figure of detection results of serum biochemical indexes of mice in Example 1 of the present application, wherein A is a figure of ALT detection results, B is a figure of AST detection results, C is a figure of TC detection results, D is a figure of TG detection results, E is a figure of LDL-C detection results, and F is a figure of HDL-C detection results; ##p<0.01, ###p<0.001, ####p<0.0001 compared with the normal group; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 compared with the model group (n=10).
[0048] Figure 5 Figure of detection results of biochemical indexes in Example 1 of the present application, wherein A is a figure of CAT detection results, B is a figure of SOD detection results, C is a figure of GSH detection results, D is a figure of GSH-pX detection results, and E is a figure of MDA detection results; ##p<0.01, ###p<0.001, ####p<0.0001 compared with the normal group; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 compared with the model group (n=10). DETAILED DESCRIPTION
[0049] The concept and the technical effects produced by the present application will be described below in combination with examples, so as to fully understand the purposes, features and effects of the present application. Obviously, the described examples are only some of the examples of the present application, but not all the examples. Based on the examples of the present application, other examples obtained by those skilled in the art without creative labor are within the protection scope of the present application.
[0050] The specific conditions not mentioned in the examples are carried out according to the conventional conditions or the conditions suggested by the manufacturers. The reagents or instruments not mentioned by the manufacturers are all conventional products that can be purchased in the market.
[0051] Example 1 Application of Jinshan taro starch in preparation of products for alcohol elimination and liver protection
[0052] In this example, an acute alcoholic liver injury model of mice induced by ethanol was constructed to verify whether Jinshan taro starch has the effect of alcohol elimination and liver protection. The specific verification method is as follows:
[0053] 1. Animals and grouping
[0054] Animal model: 70 commercially available SPF-grade C57BL male mice, aged 6-8 weeks and weighing 20-24 g were used. After one week of adaptive feeding, the mice were randomly divided into seven groups, with 10 mice in each group. The average weight of each group was approximately 23 g. The groups were as follows: (1) normal group; (2) model group; (3) silymarin group (50 mg / kg·BW); (4) Neptune Golden Zun group (150 mg / kg·BW); (5) low-dose golden yam group (75 mg / kg·BW); (6) medium-dose golden yam group (150 mg / kg·BW); and (7) high-dose golden yam group (300 mg / kg·BW).
[0055] Administration of golden yam: Take an appropriate amount of golden yam starch (commercially purchased from Enping City, Guangdong Province), add the corresponding volume of 90°C hot water according to the dosage concentration of each group, stir rapidly with a glass rod for 10 seconds to fully gelatinize, then cool to room temperature before administration.
[0056] 2. Experimental methods
[0057] (1) Construction of a 50% ethanol-induced acute alcoholic liver injury model in C57BL mice
[0058] The drug was administered orally at a dose of 0.1 mL / 10 g for 14 consecutive days. Body weights were recorded every two days. The normal and model groups were gavaged with pure water, while the remaining treatment groups were gavaged with the same dose as above. Two hours after the last dose, mice were gavaged with 50% ethanol at a dose of 0.14 mL / 10 g to induce an acute alcoholic liver injury model, except for the normal group, which was gavaged with pure water.
[0059] After 30 minutes, the drunkenness time and soberness time of the mice were recorded, and the drunkenness rate of the mice after model establishment was also recorded (drunkenness rate = number of drunk mice / total number of mice × 100%). The drunkenness of the mice was determined by whether the righting reflex disappeared. After gavage, the mice were placed with their backs facing down and gently placed in a cage. If the mice remained in the back-down position for more than 30 seconds, the righting reflex disappeared, indicating drunkenness. If the righting reflex of the drunk mice recovered and they could move freely, they were considered sober.
[0060] After excluding mice that died immediately after gavage and mice that did not show drunkenness for more than 3 hours, the number of drunk mice, drunkenness time and soberness time of each group of mice were observed and recorded.
[0061] To stabilize the model and eliminate the effects of diet, mice were gavage-treated with 50% ethanol and fasted for 16 hours before being weighed. Blood was then collected from the eyeballs and placed in a 1.5ml centrifuge tube at room temperature for at least 2 hours. The tube was then centrifuged at 3000 rpm at 4°C for 10 minutes. The supernatant was transferred to a fresh centrifuge tube as serum and stored at -80°C until further use. After blood collection, mice were sacrificed, and the liver and spleen were removed, washed in saline, and excess blood was removed. Liver morphology was photographed, and the liver and spleen were weighed to calculate the organ coefficient. A portion of the liver tissue was fixed in 4% paraformaldehyde solution, and the remaining portion was rapidly frozen in liquid nitrogen in cryovials and stored at -80°C. This was used to calculate the liver index (liver index = liver (mg) / mouse body weight (mg) × 100%).
[0062] (2) Test results
[0063] 1) Mouse weight and intoxication rate test results after modeling
[0064] The results are as follows Figure 1 As shown, from Figure 1 As shown in Figure A, weight gain in each group of mice gradually increased over the 14 days following drug administration prior to modeling, indicating that golden taro starch has no significant toxicity to mice. Following modeling with 50% ethanol orally and subsequent 16-hour fasting without food or water, the weight of the mice decreased significantly compared to the normal control group.
[0065] from Figure 1 As shown in Figure B, the drunkenness rate test results show that the drunkenness rate in the model group was significantly higher than that in the normal group, indicating that the model was successfully established. Meanwhile, the drunkenness rates in the golden yam starch-treated groups decreased to varying degrees, indicating that it has a hangover-relieving effect.
[0066] 2) Liver phenotype and liver index
[0067] The results are as follows Figure 2 As shown, from Figure 2 As shown in Figure A, in the ethanol-induced acute alcoholic liver injury model group, the liver was clearly white and enlarged, with a noticeable granular texture. However, the whitening of the liver surface was effectively alleviated and the granular texture was reduced in mice pretreated with golden yam starch.
[0068] from Figure 2 As can be seen in Figure B, compared with the normal group, the liver index of the model group was significantly increased (p<0.0001), while the liver index of the high-dose taro starch treatment group was significantly decreased (p<0.01).
[0069] 3) Detection of alcohol-detoxifying enzymes.
[0070] Experimental method: Cut 20-50mg of liver tissue and place it in a 1.5ml centrifuge tube. Add the homogenization medium extract at a ratio of 1:9 between tissue and normal saline. Use a manual tissue homogenizer to prepare a 10% liver homogenate. Measure the ADH and ALDH enzyme activities in sequence according to the kit instructions.
[0071] The results are as follows Figure 3 As shown in the figure, compared with the normal group, the activities of ADH and ALDH enzymes in the model group were significantly reduced (p<0.01, p<0.0001), while the activities of ADH and ALDH enzymes in the golden taro starch treatment group were significantly increased, and the effect was dose-dependent; this shows that golden taro starch can increase the activities of ADH and ALDH enzymes and accelerate the metabolism of ethanol in mice.
[0072] 4) Detection of mouse serum biochemical indicators
[0073] Experimental method: Mouse serum was obtained and diluted with normal saline for a certain multiple before direct testing; AST, ALT, TC, TG, LDL-C and HDL-C were determined according to the operating instructions of the Nanjing Jiancheng test kit.
[0074] The results are as follows Figure 4 As shown in the figure, compared with the normal group, the AST, ALT, TC, TG, and LDL-C levels in the model group were significantly increased (p<0.01), and HDL-C was significantly decreased (p<0.0001). In the golden yam starch-treated group, ALT and AST activities were significantly decreased; TC, TG levels, and LDL-C content were significantly decreased; and HDL-C content was increased. This indicates that golden yam starch can improve ethanol-induced acute alcoholic liver damage and abnormal lipid accumulation in mice.
[0075] 5) Detection of mouse liver biochemical indicators
[0076] Experimental method: 20-50 mg of liver tissue was cut and placed in a 1.5 ml centrifuge tube. Normal saline was added as a homogenization medium at a ratio of 1:9 between tissue and normal saline. A 10% liver homogenate was prepared using a manual tissue homogenizer. The liver homogenate was diluted a certain number of times with normal saline to obtain the optimal detection concentration, and then used for the detection of biochemical indicators. The enzyme activity levels of CAT, SOD, GSH, GSH-Px and the content of MDA were measured in sequence according to the operating instructions of the kit.
[0077] The results are as follows Figure 5As shown in the figure, compared with the normal group, the enzyme activities of CAT, SOD, GSH, and GSH-Px in the liver of the model group were significantly reduced (p<0.01), and the MDA level was significantly increased (p<0.0001). Treatment with golden yam starch significantly increased the enzyme activities of CAT, SOD, GSH, and GSH-Px, and reduced the MDA content. These results suggest that golden yam starch can protect the liver from damage by enhancing antioxidant activity.
[0078] Golden mountain taro, scientific name is banana taro ( Canna indica 'Edulis'), also known as banana lotus root, ginger taro, and dry lotus root, is a herbaceous plant of the genus Canna in the family Cannaceae. According to the "Compendium of Materia Medica," banana taro is sweet and cooling in nature, with heat-clearing, dampness-removing, and detoxifying properties. Golden yam, a Guangdong folk edible resource, is one of the most commonly grown crops for starch extraction in rural Guangdong, China. Its main components include carbohydrates, protein, amino acids, and alkaloids. Golden yam starch, extracted from golden yam, is a specialty of Enping City, Guangdong Province, and its production technique has been included in the seventh batch of Enping City's list of representative items of intangible cultural heritage. Locals often boil golden yam starch with an appropriate amount of water to form a paste for consumption. It has a delicate texture and beauty-enhancing properties, and is known as the "local bird's nest" by Enping residents. However, the alcohol-detoxifying and liver-protecting activities of golden yam starch have not been reported. This study is the first to demonstrate that golden yam starch can improve alcohol-induced acute alcoholic liver injury.
[0079] While the embodiments of the present invention have been described in detail above with reference to the accompanying drawings, the present invention is not limited to the embodiments described above. Various modifications may be made within the scope of knowledge possessed by a person skilled in the art without departing from the spirit of the present invention. Furthermore, the embodiments of the present invention and the features thereof may be combined with one another unless there is a conflict.
Claims
1. The application of golden taro starch as the sole active ingredient in the preparation of products for treating liver damage caused by drinking.
2. The use according to claim 1, characterized in that The product also includes pharmaceutically acceptable excipients; The pharmaceutically acceptable excipients include at least one of a diluent, a binder, a disintegrant, an absorption promoter, a surfactant, an adsorption carrier, a lubricant, a sweetener and a flavoring agent.
3. The use according to claim 1, characterized in that The dosage forms of the product are tablets, capsules, granules, pills, oral liquids, dry suspensions, dry extracts, injections, and transdermal preparations.
4. The use according to claim 1, characterized in that The mass fraction of the golden taro starch in the product is 0.01% to 100%.
Citation Information
Patent Citations
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