Pediococcus acidilactici PA27 capable of degrading alcohol and improving alcoholic nerve injury and application thereof

Abstract

The invention relates to pediococcus acidilactici PA27 capable of degrading alcohol and improving alcoholic nerve injury and application of the pediococcus acidilactici PA27, the pediococcus acidilactici PA27 is preserved in China General Microbiological Culture Collection Center (CGMCC), and the preservation number is CGMCC NO.31922. The pediococcus acidilactici PA27 can degrade alcohol and improve alcoholic nerve injury. The pediococcus acidilactici PA27 separated and screened by the invention can grow and propagate in an alcohol-containing culture medium, can degrade alcohol and can generate ethanol dehydrogenase and acetaldehyde dehydrogenase; the polypeptide can be used for constructing a blood-brain barrier and reducing the damage of alcohol to central nervous cells; the traditional Chinese medicine composition can reduce the expression of inflammatory cytokines TNF-alpha, inhibit the activation of astrocytes, promote the expression of brain-derived neurotrophic factors BDNF, regulate the release of alcohol-induced astrocyte neurotransmitters and improve alcoholic nerve injury.

Description

Technical Field

[0001] The invention belongs to the technical field of microbial application, and particularly relates to Pediococcus acidilactici PA27 capable of degrading alcohol and improving alcoholic nerve damage and application thereof. Background Art

[0002] Alcohol plays an important role in social, cultural and commercial activities. There are a large number of drinkers worldwide. However, excessive drinking can cause headaches, dizziness, nausea, vomiting and other discomfort symptoms. In severe cases, it can also lead to alcohol dependence and alcoholic brain damage. Ethanol causes direct and indirect damage to the brain through the blood-brain barrier, interferes with hippocampal neurogenesis, reduces synaptic plasticity, and promotes neuroinflammatory response through oxidative stress, neuroimmune signaling, microbial-gut-brain axis induction, inhibits the expression of neurotrophic factors and endogenous neuropeptides, affects brain memory and learning ability, and in severe cases, changes the structure and function of the brain, and eventually develops into cognitive impairment and neurodegenerative diseases. Therefore, people are in urgent need of alcohol sobering products that can effectively degrade alcohol and improve alcoholic nerve damage.

[0003] The alcohol sobering products on the market mainly include chemical synthetic drugs, natural Chinese herbal medicines, etc., but these products have certain limitations and cannot fundamentally reduce the body's absorption of ethanol, and some even have side effects. There are a large number of microbial flora in the human intestine, which are closely related to human health. Studies have found that intestinal flora can participate in the metabolism of alcohol. Therefore, it is very important to screen microbial strains that can degrade alcohol and improve alcoholic nerve damage from human feces, and use them in products that sober up and improve alcoholic nerve damage. Summary of the invention

[0004] The purpose of the present invention is to overcome the defects in the prior art and provide a Pediococcus acidilactici PA27 capable of degrading alcohol and improving alcoholic nerve damage and its application. The Pediococcus acidilactici PA27 can degrade alcohol, produce alcohol dehydrogenase and acetaldehyde dehydrogenase, and construct a blood-brain barrier. After the intervention of Pediococcus acidilactici PA27, the damage of alcohol to glial cells in the central nervous system can be reduced, and the alcoholic nerve damage caused by heavy drinking can be improved.

[0005] To achieve the above purpose, the technical solution adopted by the present invention is as follows:

[0006] A lactic acid bacteria PA27, deposited in the General Microbiology Center of China Microorganism Culture Collection Administration, with the deposit number CGMCC NO.31922, the deposit address: Institute of Microbiology, Chinese Academy of Sciences, No. 3, Yard 1, Beichen West Road, Chaoyang District, Beijing, and the deposit date is September 10, 2024.

[0007] As a further technical solution, the lactic acid Pediococcus PA27 is isolated and screened from fecal samples of healthy adults.

[0008] A microbial agent comprising the Pediococcus acidilactici PA27 as claimed in claim 1.

[0009] A fermentation product is obtained by fermenting the Pediococcus acidilactici PA27.

[0010] The application of the Pediococcus acidilactici PA27, the microbial agent or the fermentation product in preparing products for degrading alcohol and improving alcoholic nerve damage.

[0011] As a further technical solution, the Pediococcus acidilactici PA27 can grow and reproduce in a culture medium containing alcohol, can degrade alcohol, and can produce alcohol dehydrogenase and acetaldehyde dehydrogenase.

[0012] As a further technical solution, the lactic acid bacteria PA27 can be used to construct a blood-brain barrier and prevent alcohol-induced neurological damage.

[0013] As a further technical solution, the lactic acid bacteria PA27 can reduce the levels of inflammatory cytokines TNF-α and GFAP, inhibit the activation of astrocytes, promote the expression of brain-derived neurotrophic factor BDNF, regulate the release of alcohol-induced astrocyte neurotransmitters, and improve alcoholic nerve damage.

[0014] As a further technical solution, the product includes food, medicine, health care product or functional food.

[0015] Compared with the prior art, the present invention has the following beneficial effects:

[0016] 1) The lactic acid Pediococcus PA27 isolated and screened by the present invention is derived from fecal samples of healthy adults. Compared with chemically synthesized drugs in traditional technologies, it is safe and healthy, with almost no side effects.

[0017] 2) The isolated and screened Pediococcus acidilactici PA27 of the present invention can grow and reproduce in an alcohol-containing culture medium, can degrade alcohol, and can produce alcohol dehydrogenase and acetaldehyde dehydrogenase; can be used to construct a blood-brain barrier and reduce the damage of alcohol to central nervous cells; can reduce the expression of inflammatory cytokine TNF-α, inhibit the activation of astrocytes, can promote the expression of brain-derived neurotrophic factor BDNF, can regulate the release of alcohol-induced astrocyte neurotransmitters, and improve alcoholic nerve damage. BRIEF DESCRIPTION OF THE DRAWINGS

[0018] Figure 1 It is a schematic diagram of the structure of the Transwell chamber;

[0019] exist Figure 1 Middle, 1, Transwell chamber, 2, upper culture medium (bacterial suspension), 3, endothelial cells, 4, collagen gel, 5, polycarbonate membrane, 6, lower culture medium (C8-D1A cells);

[0020] Figure 2 This is the leak test result of Pediococcus acidilactici PA27;

[0021] Figure 3 To measure the anti-leakage performance of Transwell chamber;

[0022] exist Figure 3 In the figure, a: the result of applying the culture solution of the lower chamber of Transwell to strain PA27; b: the result of applying the culture solution of the upper chamber of Transwell to strain PA27; c: the result of applying the culture solution of the lower chamber of Transwell to strain LGG; d: the result of applying the culture solution of the upper chamber of Transwell to strain LGG;

[0023] Figure 4 To investigate the effect of Pediococcus acidilactici PA27 on the release of inflammatory factors from astrocytes induced by alcohol;

[0024] Figure 5 The effect of Pediococcus acidilactici PA27 on the release of brain-derived neurotrophic factor from astrocytes induced by alcohol;

[0025] Figure 6 The effect of Pediococcus acidilactici PA27 on alcohol-induced astrocyte neurotransmitter release;

[0026] exist Figure 6 Middle, A: GABA; B: DA; C: 5-HT;

[0027] Figure 7 To investigate the effect of Pediococcus acidilactici PA27 on alcohol-induced glial fibrillary acid protein release in astrocytes. DETAILED DESCRIPTION

[0028] The technical solution of the present invention will be clearly and completely described below in conjunction with specific embodiments. Obviously, the described embodiments are part of the embodiments of the present invention, rather than all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without creative work are within the scope of protection of the present invention.

[0029] In addition, it should be noted that the terms "comprises", "includes" or any other variations thereof are intended to cover non-exclusive inclusion, so that a process, method, article or apparatus that includes a series of elements includes not only those elements, but also other elements not explicitly listed, or also includes elements inherent to such process, method, article or apparatus.

[0030] Example 1: Isolation of strains

[0031] Feces from people who drink regularly and those who don't drink regularly were collected and placed in MRS medium for anaerobically culture. 1 mL of culture solution was diluted with 9 mL of sterile saline solution, and then spread on MRS solid medium containing 8% alcohol and cultured at 37°C for 72 hours. MRS plates with single colonies were selected, and colonies of different sizes, colors, and states were picked for Gram staining. Gram-positive bacteria were inoculated into MRS liquid medium and cultured at 37°C until turbidity. The bacterial liquid was separated by streaking in MRS solid medium, and this was repeated more than 3 times to obtain several strains with consistent colony and bacterial morphology, which were then preserved.

[0032] Example 2, strain screening and identification

[0033] The isolated strains were subjected to alcohol degradation test and acetaldehyde dehydrogenase and ethanol dehydrogenase production test to screen out strains with high alcohol degradation rate and high production of acetaldehyde dehydrogenase and alcohol dehydrogenase. The results are shown in Table 1.

[0034] 1. Test methods

[0035] 1. Alcohol degradation test:

[0036] Take the isolated strains and activate them for three generations. Inoculate the activated single strains in a modified MRS solution with an alcohol concentration of 20% at an inoculum of 4%. After culturing for 48 hours, use a refractometer to detect the alcohol concentration of each tube. Each group has three replicates, and the modified MRS solution with an alcohol concentration of 20% without bacterial solution is used as the control group.

[0037] 2. Tests for acetaldehyde dehydrogenase and ethanol dehydrogenase production:

[0038] The isolated strain was inoculated into MRS medium at an inoculum volume of 4% and cultured for 16 h. The supernatant was removed by centrifugation and the bacteria were washed three times with sterile saline to adjust the viable cell count to 5 × 10 6 CFU / mL was added with 1 ml of lysis buffer and ultrasonically disrupted (ice bath, 200 W, ultrasonic for 3 seconds. 10 seconds interval, repeated 30 times), centrifuged at 12000 rpm and 4°C for 10 minutes, and the supernatant was taken for acetaldehyde dehydrogenase and alcohol dehydrogenase production determination.

[0039] 2. Test results

[0040] Table 1 Ability of isolated strains to produce ethanol dehydrogenase, acetaldehyde dehydrogenase and degrade alcohol content

[0041] Test strains Alcohol dehydrogenase (nmol / min / ml) Aldehyde dehydrogenase (nmol / min / ml) 48h degradation of alcohol content 1-4 16.33 2.32 4.5 2-3 22.67 2.13 4.5 3-2 27.49 2.70 6 2-2 20.87 2.32 3 4-1 16.40 2.74 4 5-4 16.36 2.32 4.5 7-4 23.54 1.43 3.5 9-3 18.43 2.00 4 10-4 20.27 3.53 4 6-2 16.36 2.28 4 8-2 16.36 2.54 3

[0042] Taking into account the ability to degrade alcohol, produce acetaldehyde dehydrogenase and produce ethanol dehydrogenase, strain 3-2 has a relatively good effect, and subsequent research will focus on this strain.

[0043] The strain 3-2 was sequenced by 16s rDNA, and its nucleotide sequence was shown in SEN ID NO.1. It was identified that the strain 3-2 belonged to Pediococcus acidilactici and was named Pediococcus acidilactici PA27.

[0044] Example 3: Study on the application of Pediococcus acidilactici PA27 in constructing an in vitro blood-brain barrier

[0045] 1. Test methods

[0046] 1. Construction of blood-brain barrier

[0047] The blood-brain barrier (BBB) ​​is a barrier structure located between the central nervous system and the blood circulation system that has a certain ability to limit the passage of substances and regulate and maintain the stability of the central nervous system microenvironment. Figure 1 The blood-brain barrier was constructed in the transwell chamber shown in the figure. The upper chamber of the Transwell was covered with a layer of matrix gel. Human brain microvascular endothelial cells hCMEC / D3 were inoculated on the matrix gel to simulate the extracellular matrix. Mouse cerebellar astrocytes C8-D1A were inoculated in the lower chamber of the Transwell. The upper and lower layers of the Transwell chamber were used to simulate the blood-brain barrier. The test strain sample was added to the upper chamber to verify the repair effect of the test strain on astrocyte damage through the blood-brain barrier. At the same time, Lactobacillus rhamnosus LGG (a publicly available strain, publicly available) was used as a control. The results are shown in Figure 2-7 .

[0048] (1) Glue is applied to the bottom of the Transwell upper chamber

[0049] 1) Prepare 0.006 mol / L (0.36 g / L) glacial acetic acid solution: add 17.25 μL glacial acetic acid to 50 mL ddH2O, mix well, and sterilize with a 0.22 μm filter before use;

[0050] 2) Prepare 0.1 mg / mL rat tail collagen storage solution: take 0.5 mL of 5 mg / mL rat tail collagen, add 24.5 mL of 0.006 mol / L glacial acetic acid solution, mix well and store at 4°C;

[0051] 3) Preparation of working solution and Transwell coating: Transwell chamber was prepared according to 10 μg / cm 2 For coating, the rat tail collagen storage solution was diluted with glacial acetic acid solution to a 0.06 mg / mL working solution. 100 μL of collagen working solution was added to each well of the Transwell chamber to ensure that the collagen solution covered the surface of the vessel and dried at room temperature overnight.

[0052] (2) Construction of Transwell upper chamber monolayer barrier

[0053] The cultured endothelial cells hCMEC / D3 were digested with trypsin and resuspended in complete culture medium to adjust the cell concentration to 5×10 5 / mL, take 500μL and inoculate it in the upper chamber of the collagen-coated Transwell, add 1.5mL DMEM complete culture medium to the lower chamber to ensure that the liquid level inside and outside the Transwell chamber is level, change the medium once a day, and after 6 days of culture, use a resistor to detect the TEER value to reach 120-180Ω.cm 2 , conduct a liquid level difference experiment. Add cell culture fluid to the upper and lower chambers, and the liquid level in the upper chamber is higher than that in the lower chamber, forming a height difference between the liquid levels. Let it stand for 4 hours and observe the changes in the liquid level difference. If the liquid levels in the upper and lower chambers are flush, it indicates leakage and the barrier needs to be rebuilt. If the liquid level difference between the upper and lower chambers remains unchanged, it indicates that the barrier is well established and can be used for subsequent experiments.

[0054] (3) Determination of the anti-leakage performance of Transwell chamber

[0055] Take 500 μL of the test strain suspension and add it to the upper cell chamber to make the concentration of live bacteria 1.0×10 5 CFU / mL, add 1.5mL of antibiotic-free cell culture medium to the lower chamber and culture for 24h, take 200μL of each of the upper and lower chambers for coating, and observe the colony growth in the upper and lower chambers after 48h of culture. The presence of colonies in the upper chamber and no colony growth in the lower chamber indicates that the endothelial cell barrier is successfully constructed.

[0056] (4) Construction of Transwell chamber cell model

[0057] The concentration of cultured astrocytes C8-D1A was adjusted to 1.5×10 5 / mL, take 1.5mL and inoculate it in the lower chamber of Transwell and incubate it in a 37℃, 5% CO2 incubator for 24h. After the cells adhere to the wall, discard the supernatant and add 1.5mL of cell culture medium containing 200mM alcohol for induction to establish the alcohol-induced astrocyte model.

[0058] (5) Strain intervention

[0059] After incubating the alcohol-induced astrocyte model for 1 h, the Transwell upper chamber with a monolayer endothelial barrier was added, and the activated test strain was adjusted to a concentration of 1.5×10 5 CFU / mL, 500 μL was added to the upper chamber of cells for incubation, 500 μL of cell culture medium without the test strain was added to the upper chamber as the model group, and no alcohol intervention was used as the control group. The cells in each group were cultured in a 37°C, 5% CO2 incubator for 24 h.

[0060] (6) Sample testing

[0061] After 24 h of cell culture, the cell culture medium in the lower chamber was collected and centrifuged at 1000 r / min for 20 min at 4°C. The supernatant was collected and tested according to the tumor necrosis factor-α (TNF-α), brain-derived neurotrophic factor (BDNF), dopamine (DA), γ-aminobutyric acid (GABA), 5-hydroxytryptamine (5-HT), and glial fibrillary acidic protein (GFAP) kits.

[0062] 2. Test results and analysis

[0063] 1. Transwell upper chamber monolayer barrier construction results

[0064] from Figure 2 The results showed that the hBMEC monolayer could maintain a stable liquid level difference (+), while the liquid levels in the upper and lower chambers of the blank control group reached the same level (-) in a short period of time, indicating that the inoculated hBMEC monolayer had grown dense enough at this time and the monolayer barrier construction was initially successful.

[0065] 2. Transwel chamber anti-leakage performance test results

[0066] Figure 3 The results showed that a large number of colonies were formed in the upper chamber culture medium of Pediococcus acidilactici PA27, but no colonies were formed in the lower chamber culture medium, indicating that the test strain in the upper chamber would not directly penetrate the upper barrier to reach the lower layer, proving that the barrier was successfully constructed.

[0067] 3. Effects of strains on alcohol-induced astrocyte inflammatory factors

[0068] When astrocytes are activated, they release a variety of pro-inflammatory cytokines and inflammatory mediators, promoting inflammatory responses and tissue damage, and producing toxic effects on neurons. Figure 4 The results showed that compared with the control group, the content of tumor necrosis factor-α (TNF-α) in the cell culture fluid of the alcohol-induced astrocyte culture system in the model group was significantly increased, and the secretion amount was 50.4pg / mL. After the intervention of different strains, the release amount was significantly decreased compared with the model group. Among them, the secretion amount of TNF-α after intervention of Pediococcus acidilactici PA27 was 35.7pg / mL, and the improvement effect was better than 37.1pg / mL of Lactobacillus rhamnosus LGG. PA27 inhibited the activation of astrocytes by reducing the expression of proinflammatory cytokine TNF-α.

[0069] 1. Effects of strains on alcohol-induced brain-derived neurotrophic factor in astrocytes

[0070] BDNF is an important brain-derived neurotrophic factor in the nervous system. BDNF acts on certain neurons in the central and peripheral nervous systems, helping to support the survival of existing neurons and promoting the growth and differentiation of new neurons and synapses. In the brain, BDNF is active in the hippocampus, cortex, and basal forebrain, which are areas that are critical for learning, memory, and higher-order thinking. Figure 5 The results showed that compared with the control group, the BDNF content in the alcohol-induced astrocyte culture system of the model group was significantly reduced, and the BDNF secretion was 42.0pg / mL. After intervention with different strains, the release amount was significantly increased compared with the model group, among which the BDNF secretion after intervention with Pediococcus acidilactici PA27 was 83.3pg / mL, and the improvement effect was better than that of Lactobacillus rhamnosus LGG, which was 57.9pg / mL. It can be seen that Pediococcus acidilactici PA27 can improve nerve damage by regulating the expression of brain-derived neurotrophic factor.

[0071] 2. Effects of strains on alcohol-induced astrocyte neurotransmitter release

[0072] High-concentration alcohol intake can reduce excitatory neurotransmitters in the brain and increase inhibitory neurotransmitters, leading to slow movements and slurred speech, which are common symptoms of alcoholics. For example, alcohol can enhance the release of inhibitory neurotransmitters γ-aminobutyric acid (GABA) in the brain and reduce the release of excitatory neurotransmitters dopamine (DA). Figure 6The results showed that compared with the control group, the GABA content in the alcohol-induced astrocyte culture system in the model group increased and its secretion was 2.90 μmol / L, and the DA content decreased significantly and its secretion was 13.5 pg / mL. After intervention with different strains, the GABA release showed a downward trend compared with the model group, and the DA release showed an upward trend. After intervention with Pediococcus acidilactici PA27, the GABA secretion was 2.73 μmol / L and the DA secretion was 23.5 pg / mL. After intervention with Lactobacillus rhamnosus LGG, the GABA secretion was 2.68 μmol / L and the DA secretion was 14.1 pg / mL. The improvement effect of PA27 was better than that of Lactobacillus rhamnosus LGG.

[0073] Alcohol can directly act on the neuron cell membrane, changing its permeability and membrane potential. 5-hydroxytryptamine (5-HT) is synthesized and secreted by neurons. The normal electrical activity and ion balance of neurons are essential for the secretion of 5-HT. Drinking a lot of alcohol may disrupt these conditions and inhibit the ability of neurons to secrete 5-HT. Figure 6 The results showed that compared with the control group, the 5-HT content in the cell culture fluid of the alcohol-induced astrocyte culture system in the model group was significantly reduced, and its secretion was 0.55 ng / mL. After the intervention of different strains, the 5-HT release showed an upward trend compared with the model group. After the intervention of Pediococcus acidilactici PA27, the 5-HT secretion was 0.96 ng / mL, and after the intervention of Lactobacillus rhamnosus LGG, the 5-HT secretion was 0.79 ng / mL. The improvement effect of PA27 was better than that of Lactobacillus rhamnosus LGG.

[0074] In summary, after the intervention of Pediococcus acidilactici PA27 lactic acid bacteria, the disordered neurotransmitter levels will be regulated, the release of inhibitory neurotransmitter γ-aminobutyric acid will be reduced, the release of excitatory neurotransmitters dopamine and 5-hydroxytryptamine will be promoted, the body's neurotransmitters will tend to normal levels, the expression of inflammatory factors will be reduced, the secretion of brain-derived neurotrophic factor will be increased, and the brain neurological damage caused by high concentrations of alcohol will be reduced.

[0075] 3. Effects of strains on alcohol-induced astrocyte hyperproliferation

[0076] Astrocytes are a type of glial cells in the central nervous system (CNS). They are the largest and most numerous type of astrocytes, with complex functions and widespread distribution. Glial fibrillary acidic protein (GFAP) is a marker of astrocyte activation, and astrocyte activation is an important marker of neuroinflammation. Figure 7The results showed that after alcohol induction, the GFAP content of astrocytes in the model group increased significantly, and the secretion amount was 99.4pg / mL, indicating that astrocytes had been activated and the number of positive cells also increased significantly. After intervention with different strains, the GFAP level could be reduced. After intervention with Pediococcus acidilactici PA27, the GFAP secretion amount was 85.2pg / mL, and after intervention with Lactobacillus rhamnosus LGG, the GFAP secretion amount was 84.5pg / mL. Pediococcus acidilactici PA27 reduced the inflammatory activation of astrocytes induced by alcohol by inhibiting the secretion of GFAP.

[0077] In summary, the Pediococcus acidilactici PA27 of the present invention has the following functions:

[0078] 1) Pediococcus acidilactici PA27 has the ability to degrade alcohol, and the alcohol degradation degree reaches 6 degrees;

[0079] 2) Pediococcus acidilactici PA27 has the ability to produce ethanol dehydrogenase and acetaldehyde dehydrogenase, among which the content level of ethanol dehydrogenase is 27.49nmol / min / ml, and the content level of acetaldehyde dehydrogenase is 2.70nmol / min / ml;

[0080] 3) Construct a blood-brain barrier and verify the repair effect of Pediococcus acidilactici PA27 on alcohol-induced astrocyte damage. Pediococcus acidilactici PA27 inhibits the expression of proinflammatory cytokine TNF-α, thereby inhibiting astrocyte activation; regulates the secretion of brain-derived neurotrophic factor BDNF, improves the level of neurotransmitters disordered by alcohol, regulates the secretion of neurotransmitters such as dopamine (DA), γ-aminobutyric acid (GABA), and 5-hydroxytryptamine (5-HT), inhibits the secretion of glial fibrillary acid protein GFAP, reduces alcohol-induced inflammatory activation of astrocytes, and alleviates brain neurological damage caused by high concentrations of alcohol.

[0081] The above-described embodiments are only preferred embodiments of the present invention, and are not exhaustive of the feasible implementations of the present invention. For those skilled in the art, any obvious changes made thereto without departing from the principles and spirit of the present invention should be considered to be included in the scope of protection of the claims of the present invention.

Claims

1. A Pediococcus acidilactici PA27, characterized in that It is deposited in the General Microbiology Center of China Microorganism Culture Collection Administration with the accession number CGMCC NO.31922.

2. A Pediococcus acidilactici PA27 according to claim 1, characterized in that The Pediococcus acidilactici PA27 is isolated and screened from fecal samples of healthy adults.

3. A microbial agent, characterized in that: The method comprises the Pediococcus acidilactici PA27 as claimed in claim 1.

4. A fermentation product, characterized in that The product is prepared by fermenting the Pediococcus acidilactici PA27 according to claim 1.

5. Use of the Pediococcus acidilactici PA27 according to claim 1, the microbial agent according to claim 3 or the fermentation product according to claim 4 in preparing products for degrading alcohol and improving alcoholic nerve damage.

6. The use according to claim 5, characterized in that: The Pediococcus acidilactici PA27 can grow and reproduce in a culture medium containing alcohol, can degrade alcohol, and can produce alcohol dehydrogenase and acetaldehyde dehydrogenase.

7. The use according to claim 5, characterized in that: The Pediococcus acidilactici PA27 can be used to construct a blood-brain barrier and prevent alcohol-induced neurological damage.

8. The use according to claim 5, characterized in that: The lactic acid Pediococcus PA27 can reduce the levels of inflammatory cytokines TNF-α and GFAP, inhibit the activation of astrocytes, promote the expression of brain-derived neurotrophic factor BDNF, regulate the release of alcohol-induced astrocyte neurotransmitters, and improve alcoholic nerve damage.

9. The use according to claim 5, characterized in that: The products include food, medicine, health products or functional foods.

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