Application of plant starch in preparation of product for dispelling effects of alcohol and protecting liver
By using Jinshan Taro Starch in the hangover products, the problem of side effects and poor results in the treatment of acute alcoholic liver injury in the prior art is solved, and the effect of accelerating ethanol metabolism, reducing liver damage and improving lipid abnormalities is achieved.
Patent Information
- Application Number
- CN202411971884.5
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2024-12-30
- Publication Date
- 2025-03-21
- Estimated Expiration
- 2044-12-30
AI Technical Summary
The prior art has side effects in the treatment of acute alcoholic liver injury, and it is difficult to effectively alleviate liver damage caused by alcohol intake.
In the preparation of halting products, the activity of ethanol dehydrogenase and acetaldehyde dehydrogenase in the liver is improved by accelerating the metabolism of ethanol and acetaldehyde dehydrogenase, reducing the rate of drunkenness and liver damage.
Significantly accelerate ethanol metabolism, shorten drunken time, reduce liver index, improve antioxidant enzyme activity, improve abnormal lipid accumulation, reduce liver burden, and provide liver protection effects to protect the body.
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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 drinking a large amount of alcohol in a short period of time. The clinical manifestations are abnormal liver function and liver histological changes. After alcohol enters the human body, 90% is metabolized by the liver, mainly through the oxidation pathway involving alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH).
[0003] Modern treatments for alcohol-induced acute liver injury mainly involve 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 drug for the treatment of liver injury, has significant side effects, such as nausea, vomiting, abdominal pain, loss of appetite, and diarrhea. Silymarin is excreted from the liver. Long-term use of silymarin by patients may result in the inability of the liver to completely metabolize the drug, thereby increasing the burden on the liver. Therefore, it is of great significance to explore bioactive substances with hepatoprotective effects in natural resources to reduce liver damage caused by alcoholic drinking. 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 proposes an application of golden yam starch in preparing a hangover sobering product.
[0005] The 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 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 sobering product is proposed.
[0008] According to a second aspect of the present invention, a 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 between 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) Reduction of 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 vivo 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 golden taro starch.
[0024] In some embodiments of the present invention, the product is at least one of a medicine, a health product and a functional food.
[0025] In some embodiments of the present invention, the product is a medicine, and the medicine further includes a pharmaceutically acceptable excipient.
[0026] 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.
[0027] In some embodiments of the invention, the excipient comprises water.
[0028] In some embodiments of the present invention, the filler comprises at least one of starch and sucrose.
[0029] In some embodiments of the present invention, the binder includes at least one of a cellulose derivative, alginate, gelatin and polyvinyl pyrrolidone.
[0030] In some embodiments of the invention, the humectant comprises glycerin.
[0031] In some embodiments of the present invention, the disintegrant comprises at least one of agar, calcium carbonate and sodium bicarbonate.
[0032] In some embodiments of the invention, the absorption enhancer comprises a quaternary ammonium compound.
[0033] In some embodiments of the invention, the surfactant comprises cetyl alcohol.
[0034] In some embodiments of the present invention, the adsorption carrier includes at least one of kaolin and bentonite.
[0035] In some embodiments of the present invention, the lubricant includes at least one of talc, calcium stearate, magnesium stearate and polyethylene glycol.
[0036] In some embodiments of the present invention, the dosage form of the drug is in the form of solid, semi-solid or liquid, and can be an aqueous solution, non-aqueous solution or suspension.
[0037] In some embodiments of the present invention, the dosage form of the drug is tablets, capsules, soft capsules, granules, pills, oral liquids, dry suspensions, pellets, dry extracts, injections or infusions, transdermal agents, and transdermal microneedles.
[0038] In some embodiments of the present invention, the drug may be administered by any conventional method in the art, including but not limited to injection or oral administration.
[0039] In some embodiments of the present invention, the injection administration can be intravenous injection, intramuscular injection, intraperitoneal injection, intradermal injection or subcutaneous injection.
[0040] In some embodiments of the present invention, the mass fraction of the golden taro starch in the product is 0.01% to 100%.
[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 95%.
[0042] 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%.
[0043] 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 hangover 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 hangover and liver protection products. BRIEF DESCRIPTION OF THE DRAWINGS
[0044] The present invention will be further described below with reference to the accompanying drawings and embodiments, wherein:
[0045] Figure 1 The figure is a graph showing the test results of the weight and drunkenness rate of mice in Example 1 of the present invention, wherein A is a graph showing the test results of the weight of mice, and B is a graph showing the test results of the drunkenness rate, ###p<0.001 compared with the normal group; *p<0.05, **p<0.01 compared with the model group, (n=10);
[0046] Figure 2 The liver phenotype and liver index test result diagram in Example 1 of the present invention, wherein A is a liver morphology diagram, B is a liver index test result diagram, ####p<0.0001 compared with the normal group; *p<0.05, **p<0.01 compared with the model group, (n=10));
[0047] Figure 3 The results of alcohol detoxification-related enzyme detection in Example 1 of the present invention are shown in Figure 1, wherein A is the results of ADH enzyme detection, and B is the results of ALDH enzyme detection, ##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));
[0048] Figure 4: It is a test result diagram of the mouse serum biochemical indexes in Example 1 of the present invention, wherein A is a test result diagram of ALT, B is a test result diagram of AST, C is a test result diagram of TC, D is a test result diagram of TG, and E is a test result diagram of LDL-C; F is a test result diagram of HDL-C, ##p<0.01, ###p<0.001, ####p<0.0001 compared with the normal group; *p<0.05, **p<0.01, ***p<0.001 compared with the model group, (n=10);
[0049] Figure 5 The test result diagrams of the biochemical indicators in Example 1 of the present invention, wherein A is the test result diagram of CAT, B is the test result diagram of SOD, C is the test result diagram of GSH, D is the test result diagram of GSH-pX, and E is the test result diagram of MDA. ##p<0.01, ###p<0.001, ####p<0.0001 are compared with the normal group; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 are compared with the model group (n=10). DETAILED DESCRIPTION
[0050] The following will be combined with the embodiments to clearly and completely describe the concept of the present invention and the technical effects produced, so as to fully understand the purpose, characteristics and effects of the present invention. Obviously, the described embodiments are only part of the embodiments of the present invention, not all of them. Based on the embodiments of the present invention, other embodiments obtained by those skilled in the art without creative work are all within the scope of protection of the present invention.
[0051] If the specific conditions are not specified in the examples, the experiments were carried out under conventional conditions or conditions recommended by the manufacturer. If the manufacturers of the reagents or instruments are not specified, they are all conventional products that can be purchased commercially.
[0052] Example 1 Application of golden taro starch in the preparation of products for alcohol sobering up and protecting the liver
[0053] In this example, an ethanol-induced acute alcoholic liver injury model in mice was constructed to verify whether golden taro starch has the effect of sobering up and protecting the liver. The specific verification method is as follows:
[0054] 1. Animals and groups
[0055] Animal model: 70 commercially available SPF grade C57BL male mice, aged 6-8 weeks, weighing 20-24g; after one week of adaptive feeding, the mice were randomly divided into 7 groups, 10 mice in each group, and the average weight of each group was about 23g. The specific groups were: (1) normal group; (2) model group; (3) silymarin group (50mg / kg·BW); (4) Neptune Jinzun group (150mg / kg·BW); (5) golden yam low-dose group (75mg / kg·BW); (6) golden yam medium-dose group (150mg / kg·BW); (7) golden yam high-dose group (300mg / kg·BW).
[0056] Administration of golden yam: Take an appropriate amount of golden yam starch (commercially purchased from Enping City, Guangdong Province), add 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, cool to room temperature, and then administer.
[0057] 2. Experimental methods
[0058] (1) Construction of a 50% ethanol-induced acute alcoholic liver injury model in C57BL mice
[0059] The mice were given oral administration at 0.1 mL / 10 g for 14 days, and the body weight was recorded every two days. The normal group and the model group were given oral administration of pure water, and the other groups were given oral administration according to the above dosage. 2 hours after the last administration, except for the normal group who were given oral administration of pure water, the other mice were given oral administration of 50% ethanol at 0.14 ml / 10 g to create an acute alcoholic liver injury model.
[0060] After 30 minutes, the drunkenness time and soberness time of the mice were recorded, and the drunkenness rate of the mice after modeling was recorded (drunkenness rate = number of drunk mice / total number of mice × 100%). The drunkenness of the mice was determined by the disappearance of the righting reflex. After gavage, the mice were placed with their backs down and gently put into the cage. If the mice maintained the back-down posture for more than 30 seconds, it was considered that the righting reflex disappeared, indicating that the mice were drunk. If the righting reflex of the drunk mice recovered and they could move freely, they were sober.
[0061] After excluding mice that died immediately after oral 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.
[0062] In order to make the model stable and eliminate the influence of diet on modeling, the mice were weighed after fasting for 16 hours after gavage with 50% ethanol but without water. Then the eyeballs were removed and blood was placed in a 1.5ml ordinary centrifuge tube at room temperature for more than 2 hours, centrifuged at 3000rpm and 4℃ for 10 minutes, and the supernatant was placed in another new centrifuge tube as serum, which was stored at -80℃ for standby use. After blood was drawn, the mice were killed, the liver and spleen were removed, washed in physiological saline and the excess blood was absorbed, the liver morphology was photographed, and the liver and spleen were weighed for the calculation of the organ coefficient: a part of the liver tissue was fixed in 4% paraformaldehyde solution, and the rest was placed in a cryovial and quickly frozen with liquid nitrogen and stored at -80℃. It is used for the calculation of liver index (liver index = liver (mg) / mouse body weight (mg) × 100%).
[0063] (2) Test results
[0064] 1) Results of mouse weight and intoxication rate test after modeling
[0065] The results are as follows Figure 1 As shown, from Figure 1 As shown in the weight graph A, the weight of mice in each group gradually increased during the 14 days of drug administration before modeling, indicating that golden taro starch has no obvious toxicity to mice. After modeling with 50% ethanol gavage and then fasting for 16 hours without water restriction, the weight of mice decreased significantly compared with the normal group.
[0066] from Figure 1 As shown in the drunkenness rate test result chart B, compared with the normal group, the drunkenness rate of the model group increased significantly, indicating that the model was successfully established. The drunkenness rates of the golden taro starch-treated groups decreased to varying degrees, indicating that it has a hangover-relieving effect.
[0067] 2) Liver phenotype and liver index
[0068] 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 swollen, with obvious granularity. However, the whitening of the liver surface of mice pretreated with golden taro starch was effectively alleviated, and the granularity of the liver was weakened.
[0069] from Figure 2 As can be seen from 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 group treated with high-dose golden taro starch was significantly decreased (p<0.01).
[0070] 3) Detection of alcohol detoxification-related enzymes.
[0071] Experimental method: Cut 20-50 mg of liver tissue and place it in a 1.5 ml 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 10% liver homogenate. Measure the activity of ADH and ALDH enzymes in turn according to the operating instructions of the kit.
[0072] The results are as follows Figure 3 As shown in the figure, it can be seen that 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.
[0073] 4) Detection of mouse serum biochemical indicators
[0074] 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.
[0075] 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 in the model group increased significantly (p<0.01), and HDL-C decreased significantly (p<0.0001); while the ALT and AST activities in the golden yam starch treatment group decreased significantly; the TC, TG levels and LDL-C content decreased significantly; and the HDL-C content increased. This indicates that golden yam starch can improve ethanol-induced acute alcoholic liver injury and abnormal lipid accumulation in mice.
[0076] 5) Detection of biochemical indices in mouse liver
[0077] 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 mixture was diluted a certain multiple 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 determined in sequence according to the operating instructions of the kit.
[0078] The results are as follows Figure 5As shown in the figure, compared with the normal group, the enzyme activity levels 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). However, the treatment with golden yam starch can significantly increase the enzyme activity levels of CAT, SOD, GSH and GSH-Px, and reduce the content of MDA. These results show that golden yam starch can protect the liver from damage by enhancing antioxidant activity.
[0079] Golden yam, scientifically known as banana taro (Canna indica'Edulis'), also known as banana root, ginger taro, and dry root, is a herbaceous plant of the genus Canna in the family Canna. So far, the activity of golden yam starch in sobering up and protecting the liver has not been reported. This study is the first to find that golden yam starch can improve alcohol-induced acute alcoholic liver injury.
[0080] The embodiments of the present invention are described in detail above in conjunction with the accompanying drawings, but the present invention is not limited to the above embodiments. Various changes can be made within the knowledge of ordinary technicians in the relevant technical field without departing from the purpose of the present invention. In addition, the embodiments of the present invention and the features in the embodiments can be combined with each other without conflict.
Claims
1. Application of golden taro starch in the preparation of hangover relieving products.
2. Application of golden taro starch in the preparation of products for preventing and / or treating liver damage caused by drinking.
3. The use according to claim 1 or 2, characterized in that: The product has at least one of the following functions: (1) Accelerate the metabolism of ethanol and / or acetaldehyde; (2) shorten the duration of intoxication and / or sobriety; (3) Reduce the rate of drunkenness; (4) Reduce liver index; (5) Increase the activity of ADH and / or ALDH enzymes in the body; (6) reduce serum ALT and / or AST levels; (7) Increase the activity of CAT, SOD, GSH and / or GSH-Px; (8) Reduce MDA content; (9) Improve ethanol-induced abnormal lipid accumulation; (10) Prevent alcohol metabolism disorders caused by excessive alcohol intake.
4. The use according to claim 3, characterized in that: The increasing of ADH and / or ALDH enzyme activity in vivo includes increasing ADH and / or ALDH enzyme activity in the liver.
5. The use according to claim 3, characterized in that: The improvement of abnormal lipid accumulation induced by ethanol includes reducing the content of triglyceride, cholesterol, low-density lipoprotein cholesterol in serum, and / or increasing the content of high-density lipoprotein cholesterol in serum.
6. A product for sobering up or preventing liver damage caused by drinking, characterized in that: The product includes golden taro starch.
7. The product according to claim 6, characterized in that The product is at least one of a medicine, a health product and a functional food.
8. The product according to claim 7, characterized in that The product is a medicine, and the medicine also includes pharmaceutically acceptable excipients; Preferably, 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.
9. The product according to claim 8, characterized in that The dosage form of the medicine is tablet, capsule, soft capsule, granule, pill, oral liquid, dry suspension, drop pill, dry extract, injection or infusion, transdermal agent, transdermal microneedle.
10. The product according to claim 6, 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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