Application of lactobacillus paracasei ZJUIDS05 in improving alcohol metabolism and alcoholic liver disease

Abstract

The invention relates to the technical field of microorganisms, in particular to application of lactobacillus paracasei ZJUIDS05 (CGMCC (China General Microbiological Culture Collection Center) NO.20515) in preparation of a medicine for improving alcohol metabolism and alcoholic liver diseases. When the ZJUIDS05 is used for improving alcohol metabolism, the ZJUIDS05 can be used for reducing the ethanol content, ALT and AST in plasma; the metabolic capability and the oxidation resistance of the ethanol are enhanced; when the ZJUIDS05 intervention is used for improving alcoholic liver diseases, liver injury (ALT and AST levels are remarkably reduced) caused by alcohol can be remarkably improved, the content of ethanol in plasma is reduced, and the metabolic capacity and the antioxidant capacity of ethanol are enhanced.

Description

Technical Field

[0001] The invention relates to the technical field of microorganisms, and in particular to application of Lactobacillus Paracasei ZJUIDS05 in promoting alcohol metabolism and improving alcoholic liver disease. Background Art

[0002] With the improvement of social living standards and the increase of pressure, the frequency of drinking behavior in daily social activities has increased significantly, resulting in an increasing trend of alcohol-induced liver damage year by year.

[0003] Alcoholic liver disease (ALD) refers to a series of liver diseases caused by long-term heavy drinking, including alcoholic fatty liver disease (AFLD), alcoholic hepatitis (AH) and alcoholic cirrhosis (AC). The occurrence of these diseases is closely related to the toxic effects of alcohol on the liver, abnormal activation of the immune system and the damage mechanism of oxidative stress.

[0004] During alcohol metabolism, ethanol is converted into acetaldehyde by alcohol dehydrogenase (ADH), which is then converted into acetaldehyde by acetaldehyde dehydrogenase (ALDH). Acetaldehyde, as a highly reactive toxic metabolite, can induce significant oxidative stress response, causing oxidative damage to intracellular lipids, proteins, and DNA, thereby inducing apoptosis and necrosis of liver cells. In addition, alcohol causes a large number of intestinal toxins and harmful metabolites (such as ammonia, indole, and phenolic compounds) to be unable to be effectively cleared, leading to an imbalance in the intestinal microecology, promoting the overgrowth of harmful bacteria, increasing the absorption of endotoxins, and thus causing inflammation and damage to the liver. Therefore, it has important scientific significance for the development of effective intervention strategies and treatment methods.

[0005] In recent years, probiotics have received widespread attention as a beneficial microorganism that regulates intestinal microecology. Studies have found that probiotics have a protective effect on alcohol-induced liver damage by regulating intestinal flora, enhancing intestinal barrier function, and reducing endotoxin absorption. These effects of probiotics can effectively reduce the toxicity of alcohol to the liver and alleviate the progression of alcoholic liver disease. Therefore, probiotics, as an auxiliary treatment method, have potential application value in the prevention and treatment of alcoholic liver disease.

[0006] The invention of CN113337430B "A strain of Lactobacillus paracasei NSL0201 and its application" informs that the bacteria can alleviate or treat chronic alcoholic hepatoenteric diseases by inhibiting the increase of liver index or blood lipid level, the secretion of inflammatory factors, and reducing endotoxin content.

[0007] The invention of CN117286049B "A strain of Lactobacillus paracasei LP.DCRFF018 capable of improving alcoholic liver damage and its application" states that it has a mitigating effect on liver damage caused by alcohol.

[0008] The invention of CN117050909A "A probiotic fermentation product for sobering up and detoxifying and its application" informs that Lactobacillus plantarum Fd-01 can efficiently and effectively promote the absorption of alcohol, inhibit the production of acetaldehyde by alcohol metabolism, reduce alcohol accumulation, and help reduce the alcohol content in human blood, tissues, and organs, playing a role in sobering up and detoxifying.

[0009] The invention of 202011038787.2, "Lactobacillus paracasei ZJUIDS05 with antioxidant effect and its application", informs that: Lactobacillus paracasei ZJUIDS05 (CGMCC NO.20515) has strong in vivo and in vitro antioxidant capacity. It is used to prepare live bacterial preparations with antioxidant function and various products with antioxidant function. Summary of the invention

[0010] The technical problem to be solved by the present invention is to provide application of Lactobacillus paracasei ZJUIDS05 in improving alcohol metabolism and improving alcoholic liver disease.

[0011] In order to solve the above technical problems, the present invention provides the use of Lactobacillus Paracasei ZJUIDS05 (CGMCC NO.20515) in preparing a medicine for improving alcohol metabolism and improving alcoholic liver disease.

[0012] As an improvement of the application of the present invention: alcohol metabolism is alcohol metabolism after acute drinking.

[0013] As a further improvement of the application of the present invention: the alcohol metabolism efficiency in the body is improved, and the damage of alcohol to the liver is reduced.

[0014] As a further improvement of the application of the present invention:

[0015] When improving alcohol metabolism: ZJUIDS05 can reduce the ethanol content, ALT, and AST in plasma; enhance the metabolic capacity and antioxidant capacity of ethanol;

[0016] When the purpose is to improve alcoholic liver disease: ZJUIDS05 intervention can significantly improve alcohol-induced liver damage (ALT and AST levels are significantly reduced), reduce plasma ethanol content, and enhance ethanol metabolism and antioxidant capacity.

[0017] As a further improvement of the application of the present invention: comprising Pediococcus acidilactici ZJUID S05 and inactivated Pediococcus acidilactici ZJUID S05.

[0018] illustrate:

[0019] Reducing the ethanol content in plasma usually means that the body's metabolism and excretion of alcohol are accelerated, which can be regarded as a manifestation of improving the efficiency of alcohol metabolism.

[0020] The main detection indicators of acute alcohol and alcoholic liver disease are ALT and AST in plasma, which can reflect the degree of liver damage in the liver. The acute alcohol mice in this invention explore the effect of ZJUIDS05 on the alcohol metabolism of mice after a single ethanol binge, and the alcoholic liver disease explores the effect of ZJUIDS05 on the alcohol metabolism of mice after a single ethanol binge.

[0021] The Lactobacillus paracasei ZJUIDS05 of the present invention has the following advantages: the Lactobacillus paracasei ZJUIDS05 provided by the present invention has a strong ability to promote alcohol metabolism; the Lactobacillus paracasei ZJUIDS05 provided by the present invention has a strong antioxidant capacity. The dosage required for the human body can be obtained by converting the corresponding dosage of mice. BRIEF DESCRIPTION OF THE DRAWINGS

[0022] The specific implementation modes of the present invention are further described in detail below with reference to the accompanying drawings.

[0023] Figure 1 The invention discloses the effect of the (inactivated) Lactobacillus paracasei ZJUIDS05 on plasma alanine aminotransferase and aspartate aminotransferase (ALT and AST) in acute alcoholic mice;

[0024] Figure 2 The effect of the (inactivated) Lactobacillus paracasei ZJUIDS05 of the present invention on the alcohol metabolism rate of acute alcohol mice;

[0025] Figure 3 The effect of the (inactivated) Lactobacillus paracasei ZJUIDS05 of the present invention on alcohol dehydrogenase (ADH) and glutathione reductase (GR) in acute alcohol mice;

[0026] Figure 4 The present invention is the effect of the (inactivated) Lactobacillus paracasei ZJUIDS05 on plasma alanine aminotransferase and aspartate aminotransferase (ALT and AST) in chronic alcohol-fed mice;

[0027] Figure 5 The effect of the (inactivated) Lactobacillus paracasei ZJUIDS05 of the present invention on the plasma alcohol level of chronic alcohol-fed mice;

[0028] Figure 6 The invention discloses the effect of the (inactivated) Lactobacillus paracasei ZJUIDS05 on alcohol dehydrogenase (ADH) and glutathione reductase (GR) in chronic alcohol-fed mice. DETAILED DESCRIPTION

[0029] The present invention is further described below in conjunction with specific embodiments, but the protection scope of the present invention is not limited thereto:

[0030] The present invention adopts Lactobacillus Paracasei ZJUIDS05 (CGMCCNO.20515).

[0031] Example 1, preparation method of ZJUIDS05 bacterial liquid:

[0032] A single colony of Lactobacillus Paracasei ZJUIDS05 was selected and inoculated into 50 mL MRS liquid culture medium and placed in a 37°C incubator for 18 h. The colony was activated again in 250 mL MRS liquid culture medium at a 5% (volume %) inoculation amount and placed in a 37°C incubator for 24 h. Finally, the activated Lactobacillus Paracasei ZJUIDS05 was subjected to high-density anaerobic culture in a 10 L fermenter at a 5% inoculation amount and anaerobically cultured for 18 h at 37°C and pH 6.8; the bacterial solution density reached 10 9 ~10 10 CFU / mL is about the same as the bacterial solution (live bacterial solution).

[0033] Example 2, preparation method of inactivated Pediococcus acidilactici ZJUID S05 bacterial liquid:

[0034] The above-mentioned ZJUID S05 bacterial solution was inactivated at 121°C under high temperature and high pressure for 30 min to serve as the inactivated ZJUID S05 bacterial solution.

[0035] Experiment 1: Lactobacillus paracasei ZJUIDS05 promotes alcohol metabolism

[0036] 1. Experimental animals: 48 C57BL / 6 male mice were raised in the SPF environment of the Experimental Animal Center of Zhejiang Chinese Medical University. Raising environment: room temperature 20-25℃, light and dark alternation every 12 hours, relative humidity about 50%, feed, drinking water, etc. are uniformly matched, keep the indoor environment well ventilated, clean every day, and maintain a good sanitary environment in the cage. All experiments comply with the Animal Ethics Code and the relevant regulations of the Experimental Animal Ethics Committee, and are specifically carried out in accordance with IAC and other relevant standard operating procedures (SOP). After the experiment, the abdominal aorta was anesthetized and blood was collected, and the corpses were uniformly handled harmlessly.

[0037] 2. Reagents: anhydrous ethanol (CAS-NO: 64-17-5, lichrosolv), ALT kit (Cat. No.: C009-2 Nanjing Jiancheng Bioengineering Institute), AST kit (Cat. No.: C010-2 Nanjing Jiancheng Bioengineering Institute), glutathione peroxidase detection kit (Cat. No.: S0057S Biyuntian Biotechnology), alcohol dehydrogenase detection kit (Cat. No.: BC1085 Solebold).

[0038] 3. Methods: After one week of adaptation feeding in an SPF animal laboratory, 8-week-old C57BL / 6 mice were randomly divided into 4 groups, with 24 mice in each group. They were control group (Control group), alcohol group (Ethanol group), alcohol group + Lactobacillus paracasei ZJUIDS05 (Ethanol+ZJUIDS05 group), and alcohol group + inactivated Lactobacillus paracasei ZJUIDS05 (Ethanol+ZJUIDS05 (heat-killed) group).

[0039] Intervention method: All mice in each group were fed with normal control feed, and the Ethanol+ZJUIDS05 group was gavaged with 200 μL ZJUIDS05 bacterial solution (concentration of bacterial solution was 10 9 CFU / mL), the Ethanol+ZJUIDS05 (heat-killed) group was gavaged with 200μL of inactivated Lactobacillus paracasei ZJUIDS05 bacterial solution, and the Control group and Ethanol group were gavaged with 0.2ml of normal saline every day. After 4 weeks of continuous intervention, mice except the control group were given acute alcohol gavage, with a gavage dose of (5g / kg). Six hours after gavage with ethanol, 1% pentobarbital was injected intraperitoneally for anesthesia, and blood was collected from the inferior vena cava to measure plasma ethanol and other indicators.

[0040] 3.1 Gas chromatography (GC) to measure plasma ethanol content by headspace vial

[0041] The sample to be tested (mouse plasma) was diluted with ultrapure water (1:1). Shake gently. If the sample contains more impurities, centrifuge gently (4°C, 3000×g, 5 minutes) and take the supernatant. After mixing the supernatant with chromatography-grade tert-butyl alcohol (1:5), filter it with a 0.45μm disposable filter and inject it into a chromatographic bottle. The gas chromatograph includes an automatic sampler AOC-20S, a flame ionization detector (FID), a GC-2010 and an Rtx-BAC1 chromatographic column (specifications are 30m×0.32mm×1.8μm). Injection mode: split injection, split ratio 20:1, carrier gas control mode: constant linear velocity, carrier gas is nitrogen (2ml / min), injection volume 0.2μL. The column temperature program can be adjusted as follows: the initial temperature is 40°C for 2 minutes, the temperature is increased to 240°C at a rate of 10°C / min, and it is maintained for 1 minute, and the total time is 23min.

[0042] 3.2 Plasma ALT detection

[0043] Mouse plasma samples were directly sampled for determination. The matrix solution was preheated at 37°C in advance. 20 μL matrix solution and 5 μL sample to be tested were added to the sample wells and mixed. 20 μL matrix solution was added to the control wells and incubated at 37°C for 30 min. 20 μL of 2,4-dinitrophenylhydrazine solution was added to the determination wells and control wells, and 5 μL sample to be tested was added to the control wells, mixed, and incubated at 37°C for 20 min. 200 μL of 0.4 mol / L sodium hydroxide solution was added to each well, mixed, and placed at room temperature for 15 min. The OD value of each well was measured by an enzyme marker at a wavelength of 510 nm, and the standard curve was checked to obtain the corresponding ALT / GPT activity unit.

[0044] 3.3 Plasma AST detection

[0045] Mouse plasma samples were directly sampled for determination. The matrix solution was preheated at 37°C in advance. 20 μL matrix solution and 5 μL sample to be tested were added to the sample wells and mixed. 20 μL matrix solution was added to the control wells and incubated at 37°C for 30 min. 20 μL of 2,4-dinitrophenylhydrazine solution was added to the determination wells and control wells, and 5 μL sample to be tested was added to the control wells, mixed, and incubated at 37°C for 20 min. 200 μL of 0.4 mol / L sodium hydroxide solution was added to each well, mixed, and placed at room temperature for 15 min. The OD value of each well was measured by an enzyme marker at a wavelength of 510 nm, and the standard curve was checked to obtain the corresponding AST / GPT activity unit.

[0046] 3.4 Determination of liver alcohol dehydrogenase ADH content

[0047] To detect the activity of alcohol dehydrogenase (ADH), first homogenize the tissue mass (g): extract volume (mL) in a ratio of 1:5-10 (it is recommended to weigh about 0.1g of tissue and add 1mL of extract) under ice bath conditions. Then, centrifuge the homogenate at 16,000g for 20 minutes at 4°C, take the supernatant and place it on ice for testing. ADH catalyzes NADH to reduce acetaldehyde to ethanol. At the same time, NADH has an absorption peak at 340nm, and NAD+ has no absorption. The ADH activity is calculated by measuring the rate of decrease of absorbance at 340nm. Use an ELISA reader, preheat for 30 minutes in advance, set the wavelength to 340nm, and adjust to zero with distilled water. Preheat reagent 1 in a 25°C water bath for more than 30 minutes. Blank tube: Add 20μL distilled water, 8μL reagent 2, 152μL reagent 1 and 20μL reagent 3 to the 96-well plate, mix well, and measure the absorbance values ​​A1 and A2 at 15 seconds and 75 seconds at 340nm, and calculate ΔA blank tube = A1-A2. Test tube: Add 20μL supernatant instead of distilled water, repeat the above operation, record the absorbance values ​​A3 and A4 at 15 seconds and 75 seconds, and calculate ΔA test tube = A3-A4. Calculate ADH activity based on the difference between ΔA test tube and ΔA blank tube.

[0048] Description: Alcohol dehydrogenase (ADH) is a key enzyme in the metabolism of short-chain alcohols in organisms. It catalyzes the reversible conversion of ethanol and acetaldehyde and plays an important role in many physiological processes. ADH in mammals is mainly produced in the liver. Liver damage causes ADH to be released into the serum. The level of serum ADH activity reflects whether liver function is abnormal.

[0049] 3.5 Determination of liver glutathione reductase GR content

[0050] To detect glutathione reductase (GR) activity, animals were first perfused with saline containing 0.16 mg / mL heparin to remove blood. Tissue samples were then collected and homogenized at a ratio of 200 μL of lysis buffer per 20 mg of tissue. The homogenization process was performed using the TissueMaster TM Tissue grinder, completed at 4°C. After homogenization, the sample was centrifuged at 12,000×g for 10 minutes at 4°C, and the supernatant was used to detect GR activity. During the detection, the sample was reacted with oxidized glutathione (GSSG) and the chromogenic substrate DTNB, and the generated yellow TNB was linearly positively correlated with GR activity. The amount of TNB generated was measured at A412 wavelength by an ELISA reader to calculate the activity of GR. Since glutathione reductase becomes the rate-limiting factor in the reaction system, the amount of TNB generated can reflect the activity of GR.

[0051] Description: Glutathione reductase (GR) is a flavoprotein oxidoreductase widely present in eukaryotic and prokaryotic organisms and is one of the key enzymes in the glutathione redox cycle.

[0052] 4. Experimental Results

[0053] Figure 1 The results showed that Lactobacillus paracasei ZJUIDS05 could significantly reduce the increase of ALT and AST caused by acute alcohol gavage. After gavage of ethanol (5g / kg), the plasma ALT and AST levels of mice were detected (p<0.05). The results showed that compared with the Control group, the plasma ALT and AST levels of mice in the Ethanol group were significantly increased, while the ALT and AST levels of the Ethanol+ZJUIDS05 group and the Ethanol+ZJUIDS05 (heat-killed) group were significantly lower than those of the Ethanol group, indicating that ZJUIDS05 intervention can significantly improve liver damage caused by alcohol feeding.

[0054] Figure 2 The results showed that after intragastric administration of ethanol (5g / kg), the plasma ethanol content of mice in the Ethanol+ZJUIDS05 group and the Ethanol+ZJUIDS05 (inactivated) group was lower than that in the Ethanol group at 2 hours, 4 hours, and 8 hours (p<0.05). This indicates that both ZJUIDS05 and ZJUIDS05 (inactivated) bacterial solutions can accelerate the metabolism of ethanol.

[0055] Figure 3 The results showed that after intragastric administration of ethanol (5g / kg), the activities of plasma alcohol dehydrogenase (ADH) and glutathione reductase (GR) in mice in the Ethanol group were significantly reduced compared with those in the Control group; while the activities of alcohol dehydrogenase (ADH) and glutathione reductase (GR) in mice in the Ethanol+ZJUIDS05 group and the Ethanol+ZJUIDS05 (inactivated) group were significantly higher than those in the Ethanol group (p<0.05). This indicates that ZJUIDS05 and ZJUIDS05 (inactivated) bacterial solutions can enhance the metabolic capacity and antioxidant capacity of ethanol.

[0056] Experiment 2: Improvement of alcoholic liver disease by Lactobacillus paracasei ZJUIDS05

[0057] 1. Experimental animals: 48 C57BL / 6 male mice were raised in the SPF environment of the Experimental Animal Center of Zhejiang Chinese Medical University. Raising environment: room temperature 20-25℃, light and dark alternation every 12 hours, relative humidity about 50%, feed, drinking water, etc. are uniformly matched, keep the indoor environment well ventilated, clean every day, and maintain a good sanitary environment in the cage. All experiments comply with the Animal Ethics Code and the relevant regulations of the Experimental Animal Ethics Committee, and are specifically carried out in accordance with IAC and other relevant standard operating procedures (SOP). After the experiment, the abdominal aorta was anesthetized and blood was collected, and the corpses were uniformly handled harmlessly.

[0058] 2. Reagents: anhydrous ethanol (CAS-NO: 64-17-5, lichrosolv), ALT kit (Cat. No.: C009-2 Nanjing Jiancheng Bioengineering Institute), AST kit (Cat. No.: C010-2 Nanjing Jiancheng Bioengineering Institute), glutathione peroxidase detection kit (Cat. No.: S0057S Biyuntian Biotechnology), alcohol dehydrogenase detection kit (Cat. No.: BC1085 Solebold).

[0059] Lieber-DeCarli alcohol liquid model feed (product code TP4030B, Nantong Trophy Feed Technology Co., Ltd.); Lieber-DeCarli control liquid feed (product code TP4030BC, Nantong Trophy Feed Technology Co., Ltd.).

[0060] 3. Methods: After C57BL / 6 mice were adapted to feeding in an SPF animal laboratory for one week, 8-week-old C57BL / 6 mice were randomly divided into 4 groups, with 24 mice in each group. They were control feed feeding group (pair-fed, PF group), alcohol feed feeding group (alcohol-fed, AF group), alcohol feed feeding group + Lactobacillus paracasei ZJUIDS05 (AF+ZJUIDS05 group), and alcohol feed feeding group + inactivated Lactobacillus paracasei ZJUIDS05 (AF+ZJUIDS05 (heat-killed) group). The alcoholic liver disease mouse model was established by feeding with Lieber-DeCarli liquid alcohol feed, which was purchased from Nantong Trofi Feed Technology Co., Ltd. Each group of mice was adaptively fed with non-alcoholic Lieber-DeCarli control liquid feed for the first three days, and the daily liquid feed amount for each mouse was 15g. After the adaptive feeding, the PF group was fed with Lieber-DeCarli control liquid feed for 4 weeks. During this period, the volume of the control liquid feed of the PF group was adjusted according to the intake of the Lieber-DeCarli alcohol liquid model feed of the alcohol-fed group. The AF group, AF+ZJUIDS05 group and AF+ZJUIDS05 (heat-killed) group were fed with Lieber-DeCarli alcohol liquid feed for 4 weeks. The PF and AF groups were gavaged with 200 μL PBS every day, and the AF+ZJUIDS05 group and AF+ZJUIDS05 (heat-killed) group were gavaged with 200 μL Lactobacillus paracasei ZJUIDS05 and inactivated Lactobacillus paracasei ZJUIDS05 bacterial liquid. The feed consumed by the mice was changed every day and the food intake was recorded. The weight of the mice was recorded every week. After the feeding, a single ethanol gavage was given at a dose of 5 g / kg. Six hours after gavage, the mice were anesthetized with 1% pentobarbital intraperitoneal injection, and blood was taken from the inferior vena cava to measure plasma ethanol and other indicators. All experiments followed the animal ethics code and the relevant regulations of the Experimental Animal Ethics Committee, and were conducted in accordance with IAC and other relevant standard operating procedures (SOPs). After the experiment, blood was collected from the abdominal aorta under anesthesia, and the bodies were uniformly disposed of in a harmless manner.

[0061] Description: Lieber-DeCarli control liquid feed is a model feed used to study the effects of alcohol (ethanol) on the metabolism of various nutrients in organisms. Lieber-DeCarli alcohol liquid model feed is a feed with alcohol added to the control liquid feed. Since the feed is a liquid feed, it is weighed every day and the amount of feed given the next day is adjusted according to the amount of food consumed the previous day. This is common sense.

[0062] The following items were tested according to the test method described in Experiment 1 above:

[0063] 3.1 Gas chromatography (GC) was used to measure plasma ethanol content through headspace vials;

[0064] 3.2 Plasma ALT detection;

[0065] 3.3 Plasma AST detection;

[0066] 3.4 Determination of liver alcohol dehydrogenase ADH content;

[0067] 3.5 Determination of liver glutathione reductase GR content;

[0068] 4. Experimental Results

[0069] Figure 4 The results showed that Lactobacillus paracasei ZJUIDS05 can improve liver damage caused by alcohol feeding. The plasma ALT and AST levels of mice in the AF group were significantly higher than those in the PF group, while the ALT and AST levels in the AF+ZJUIDS05 group and the AF+ZJUIDS05 (heat-killed) group were significantly lower than those in the AF group, indicating that ZJUIDS05 intervention can significantly improve liver damage caused by alcohol feeding.

[0070] Figure 5 The results showed that Lactobacillus paracasei ZJUIDS05 could accelerate the metabolism of alcohol. Compared with the PF group, the ethanol content in the plasma of mice in the AF group was significantly increased, and the intervention of ZJUIDS05 could significantly reduce the ethanol content in the plasma of mice.

[0071] Figure 6 The results showed that Lactobacillus paracasei ZJUIDS05 could improve the metabolic capacity and antioxidant capacity of alcohol. The results showed that compared with the PF group, alcohol feeding led to a significant decrease in the activities of plasma alcohol dehydrogenase (ADH) and glutathione reductase (GR) in mice; while the activities of alcohol dehydrogenase (ADH) and glutathione reductase (GR) in the AF+ZJUIDS05 group and the AF+ZJUIDS05 (inactivated) group were significantly higher than those in the AF group (p<0.05). This shows that ZJUIDS05 and ZJUIDS05 (inactivated) bacterial liquid can enhance the metabolic capacity and antioxidant capacity of ethanol.

[0072] Comparative Example 1: Lactobacillus paracasei NSL0201 and Lactobacillus paracasei LP.DCRFF018 were tested according to Experiment 1, and the experimental results were compared with those of the present invention as follows:

[0073] The ZJUIDS05 of the present invention can reduce the increase of the plasma ethanol content of mice induced by alcohol, and can increase the activities of alcohol dehydrogenase and glutathione reductase in mice; while the bacterial liquid experimental results of Lactobacillus paracasei NSL0201 and Lactobacillus paracasei LP.DCRFF018 cannot reflect the above performance.

[0074] Comparative Example 2: Lactobacillus plantarum Fd-01 was subjected to experiment 2, and the experimental results were compared with those of the present invention as follows:

[0075] The ZJUIDS05 of the present invention can improve alcohol-induced liver damage in mice, accelerate the metabolism of alcohol, and reduce the levels of ALT and AST in mouse plasma; while the experimental results of Lactobacillus plantarum Fd-01 cannot reflect the above performance.

[0076] Finally, it should be noted that the above examples are only some specific embodiments of the present invention. Obviously, the present invention is not limited to the above embodiments, and there are many variations. All variations that can be directly derived or associated with the content disclosed by a person skilled in the art should be considered as the protection scope of the present invention.

Claims

1. Application of Lactobacillus paracasei ZJUIDS05 in the preparation of drugs for improving alcohol metabolism and alcoholic liver disease.

2. The use according to claim 1, characterized in that: Alcohol metabolism is the metabolism of alcohol after acute drinking.

3. The use according to claim 1 or 2, characterized in that: Improve the efficiency of alcohol metabolism in the body and reduce alcohol damage to the liver.

4. The use according to claim 3, characterized in that At least one of the following: When improving alcohol metabolism: ZJUIDS05 can reduce the ethanol content, ALT, and AST in plasma; enhance the metabolic capacity and antioxidant capacity of ethanol; When the purpose is to improve alcoholic liver disease: ZJUIDS05 intervention can improve alcohol-induced liver damage, reduce plasma ethanol content, and enhance ethanol metabolism and antioxidant capacity.

5. The use according to any one of claims 1 to 4, characterized in that: Including Pediococcus acidilactici ZJUID S05 and inactivated Pediococcus acidilactici ZJUID S05.

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