Application of combination of nicotinic acid and bifidobacterium subsp. Lactis F1-7 in preparation of medicine for treating and / or preventing alcoholic fatty liver

Abstract

The invention discloses an application of combination of nicotinic acid and bifidobacterium subsp. Lactis F1-7 in preparation of a medicine for treating and / or preventing alcoholic fatty liver, and relates to the technical field of treatment and prevention of alcoholic fatty liver. According to the invention, a mouse AFLD model is established through alcohol feeding, intervention of nicotinic acid and animal bifidobacterium subsp. Lactis F1-7 is given, and a key target GPR109A is taken as a basis for treating and / or preventing alcoholic fatty liver. It is found through observation that compared with independent use of the two, combined application of the two can significantly reduce the liver index, reverse liver injury, significantly reduce serum inflammatory factors and improve expression of intestinal barrier related proteins, and a theoretical basis is laid for subsequent research and development of drugs.

Description

Technical Field

[0001] The present invention relates to the technical field of treatment and prevention of alcoholic fatty liver, and more particularly to the use of niacin in combination with Bifidobacterium lactis subsp. F1-7 in the preparation of a medicament for treating and / or preventing alcoholic fatty liver. Background Art

[0002] Drinking alcohol can cause damage to health, especially increasing damage to the liver. After being absorbed by the gastrointestinal tract, the alcohol ingested by the human body is distributed throughout the body, where the liver plays an important role as the body's largest detoxification organ. The liver's earliest reaction to alcohol is mainly fatty degeneration, which is characterized by the accumulation of fat (mainly triglycerides, phospholipids and cholesterol esters) in liver cells. In addition to damaging the liver, long-term drinking can also damage intestinal function and affect intestinal flora. Studies have shown that most patients with liver disease have an imbalance in the intestinal microecology, and the degree of imbalance is closely related to the severity of liver disease. Long-term alcohol intake by the human body destroys the intestinal barrier and the balance of the flora, increases intestinal permeability, causes the displacement of harmful substances such as endotoxins, produces a large number of inflammatory factors and aggravates liver damage. Therefore, paying attention to intestinal health and flora balance plays a key role in alcoholic liver disease.

[0003] Niacin, also known as vitamin B3, is widely found in many natural foods. Niacin has excellent lipid-lowering properties and has been used clinically for many years as a lipid-lowering agent. However, high doses of niacin can cause flushing, so interventional niacin intake needs to be maintained within a safe range. Niacin has a high affinity for G-protein-coupled receptor 109A (GPR109A), often acting on this receptor to regulate lipid metabolism. A study by Ye et al. explored the effects of niacin on non-alcoholic fatty liver disease and found that niacin can inhibit liver lipogenesis in mice through a GPR109A-mediated signaling pathway. In addition to niacin's agonistic effects on GPR109A, short-chain fatty acids (SCFAs) produced by the gut microbiota can also act on this receptor and exert regulatory effects.

[0004] Alcohol damages the intestines before it affects the liver. Excessive alcohol consumption can damage the intestinal barrier, affecting the intestinal microbiota and leading to deficiencies in short-chain fatty acids and trace elements. Alterations in the intestinal microbiome can affect normal intestinal function and liver lipid metabolism in multiple ways. Previous studies have shown that probiotic supplementation can improve a damaged intestinal barrier and replenish SCFAs, reducing liver damage in alcoholic animal models. Bifidobacterium animalis subsp. lactis F1-7 is a probiotic strain with anti-inflammatory and lipid-lowering properties that can modulate the intestinal microbiota. Previous studies have demonstrated that this strain regulates lipid metabolism and can influence the abundance and composition of the intestinal microbiota. Currently, research on the combined effects of niacin and probiotics on alcoholic liver injury is extremely limited. Therefore, it is worth investigating whether niacin and Bifidobacterium animalis subsp. lactis F1-7 can affect liver damage and lipid metabolism in AFLD mice through the target GPR109A. Summary of the Invention

[0005] In view of this, the present invention provides use of niacin in combination with Bifidobacterium lactis subsp. F1-7 in the preparation of a medicament for treating and / or preventing alcoholic fatty liver.

[0006] In order to achieve the above object, the present invention adopts the following technical solutions:

[0007] Use of niacin in combination with Bifidobacterium lactis subsp. F1-7 in the preparation of a medicine for treating and / or preventing alcoholic fatty liver.

[0008] Preferably, niacin is used in combination with Bifidobacterium lactis subsp. F1-7 to improve its intestinal barrier and increase the expression of key barrier proteins ZO-1, Claudin-1 and Occludin.

[0009] Preferably, niacin is used in combination with Bifidobacterium lactis subsp. F1-7 to improve alcohol-induced serum lipid disorders, reduce the TC and TG levels in the serum of mice with alcoholic fatty liver, increase the HDL-C level in the serum of mice, and reduce the LDL-C level.

[0010] Preferably, niacin is used in combination with Bifidobacterium lactis subsp. F1-7 to reverse liver damage in mice with alcoholic fatty liver disease and reduce serum ALT and AST levels.

[0011] Preferably, niacin is used in combination with Bifidobacterium lactis subspecies F1-7 to reduce the level of serum inflammatory factors in mice with alcoholic fatty liver disease; the inflammatory factors are LPS, TNF-α, IL-6, and IL-1β.

[0012] Preferably, niacin is used in combination with Bifidobacterium lactis subsp. F1-7 to improve lipid accumulation in liver cells of mice with alcoholic fatty liver disease and reduce TC and TD levels in the liver.

[0013] A medicine for treating and / or preventing alcoholic fatty liver, comprising niacin and Bifidobacterium lactis subspecies F1-7.

[0014] It can be seen from the above technical solution that, compared with the prior art, the present invention establishes an AFLD model in mice by alcohol feeding, administers niacin and animal Bifidobacterium lactis subsp. F1-7 intervention, and evaluates the changes in the intestinal flora of mice and the improvement of the intestinal tract by animal Bifidobacterium lactis subsp. F1-7 starting from the key target GPR109A, so as to better understand the protective effect of the intervention in this study on AFLD in mice. BRIEF DESCRIPTION OF THE DRAWINGS

[0015] In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the following briefly introduces the drawings required for use in the embodiments or the description of the prior art. Obviously, the drawings described below are merely embodiments of the present invention. For ordinary technicians in this field, other drawings can be obtained based on the provided drawings without paying any creative work.

[0016] Figure 1 Effects of niacin and animal Bifidobacterium lactis subsp. F1-7 on serum indicators of liver injury in mice; (A) serum ALT; (B) serum AST; the histograms marked with different letters are significantly different, p<0.05.

[0017] Figure 2 Effects of niacin and Bifidobacterium animalis subsp. lactis F1-7 on lipid metabolism levels in mice; (A) serum TC; (B) serum TG; (C) serum HDL-C; (D) serum LDL-C; the differences in histograms marked with different letters are significant, p<0.05.

[0018] Figure 3 Effects of niacin and Bifidobacterium animalis subsp. lactis F1-7 on the levels of serum inflammatory factors in mice; (A) serum LPS; (B) serum TNF-α; (C) serum IL-6; (D) serum IL-1β; the differences in histograms marked with different letters are significant, p<0.05.

[0019] Figure 4 Indicators of liver tissue pathological changes and liver lipid levels in mice; (A) HE staining and Oil Red O staining of liver tissue (200×); (B) liver TC; (C) liver TG; The histograms marked with different letters are significantly different, p<0.05.

[0020] Figure 5Immunofluorescence staining and fluorescence intensity of GPR109A in mouse liver tissue. (A) Immunohistochemical staining of mouse liver protein GPR109A (200×); (B) Quantitative analysis of GPR109A-positive areas. Different letters indicate significant differences, p < 0.05.

[0021] Figure 6 Effects of niacin and Bifidobacterium animalis subsp. lactis F1-7 on the expression of key intestinal barrier proteins in mice; (A) Immunohistochemical staining of key intestinal barrier proteins ZO-1, Claudin-1, and Occludin in mice (200×); (B) Quantitative analysis of the positive areas for ZO-1, Claudin-1, and Occludin. Different letters indicate significant differences, p < 0.05.

[0022] Figure 7 Effects of niacin and Bifidobacterium animalis subsp. lactis F1-7 on the intestinal flora of mice; (A) Community structure analysis at the genus level; (B) Relative abundance of Akkermansia; Different letters indicate significant differences, p < 0.05 DETAILED DESCRIPTION

[0023] The following will clearly and completely describe the technical solutions in the embodiments of the present invention in conjunction with the accompanying drawings. Obviously, the described embodiments are only part of the embodiments of the present invention, not all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without making creative efforts are within the scope of protection of the present invention.

[0024] Strain culture

[0025] The strain used in the embodiment is Bifidobacterium animalis subsp. lactis F1-7 (deposit number: CCTCC NO: M 2020833, deposit date December 2, 2020, deposit address: Wuhan University, Wuhan, China, classified as Bifidodocterium animails subsp F1-7), and stored in the Nutrition and Food Hygiene Teaching and Research Section. The frozen Bifidobacterium animalis subsp. lactis F1-7 was taken out and inoculated into the prepared MRS medium and cultured at a constant temperature of 37°C for 48h. After the strain was activated twice, the bacterial solution was centrifuged at 5000×g for 15min, the supernatant was removed to obtain the bacterial precipitate, and then washed twice with sterile phosphate buffered saline (PBS). The total viable count was adjusted to 1×10 by the colony counting method. 9 CFU / mL, and the bacterial suspension was stored at 4°C until use.

[0026] experimental animals

[0027] The experimental animals were 75 healthy, 8-week-old, SPF-grade male C57BL / 6N mice (20 ± 2 g) purchased from Beijing Weitonglihua Laboratory Animal Technology Co., Ltd. (License No. SYXK(Lu)20200009). Mice were individually housed in a room maintained under constant conditions: temperature (21-25°C), humidity (50-60%), and a 12-h light / dark cycle. All animal experimental protocols were conducted in accordance with the guidelines of the Institutional Animal Ethics Committee and approved by the Animal Care and Use Committee of Qingdao University School of Medicine (QDU-AEC-2022054).

[0028] Example 1

[0029] Animal grouping and intervention

[0030] 75 mice were fed with complete feed and free access to water. After 1 week of adaptation, the mice were randomly divided into 5 groups (15 mice in each group):

[0031] Control group (control): fed with 4% Lieber-DeCarli liquid feed;

[0032] The alcohol model group (AFLD), niacin intervention group (NA), Bifidobacterium animalis subsp. lactis F1-7 intervention group (F1-7), and niacin and Bifidobacterium animalis subsp. lactis F1-7 mixed intervention group (NF) were all given 4% Lieber-DeCarli alcohol liquid feed.

[0033] Among them, the Control group and the AFLD group were given 5 mL·kg -1 ·d -1 PBS was administered orally; NA group was given 50 mg·kg -1 ·d -1 Nicotinic acid was administered orally; F1-7 group was given 1×10 9 CFU / mL bacterial solution was administered orally; NF group was given 50 mg·kg -1 and 1×10 9 The mice in each group were given free access to food and water. Their body weight was recorded weekly, and their condition and survival were observed.

[0034] Sample collection and processing

[0035] After the last oral gavage at the end of the 8th week, fresh feces were collected from each group of mice. All mice were fasted but not watered for 12 hours, and after being weighed, they were anesthetized by intraperitoneal injection of 40 mg / kg sodium pentobarbital. After the mice were anesthetized, their eyeballs were removed for blood collection, and then they were killed by spinal dislocation and their tissues and organs were separated. The obtained serum was centrifuged and used for biochemical index detection; after the liver tissue was weighed, part of it was fixed in 4% paraformaldehyde for subsequent histopathological observation; the ileum and colon tissues were separated and partly fixed; and the intestinal contents were collected in sterile centrifuge tubes. All collected mouse serum, liver, intestine and other tissue samples were quickly frozen in liquid nitrogen and then transferred to a -80°C refrigerator for storage pending subsequent index detection.

[0036] Example 2 Body weight and liver index determination

[0037] Throughout the experiment, the weight of each group of mice was recorded weekly. The livers of mice were removed and weighed immediately after sacrifice. The liver index was calculated using the formula: Liver index (%) = liver weight (g) / body weight (g).

[0038] Results showed that mice in all groups were in good general condition during the adaptive feeding period, with normal water and food intake. After liquid feeding, mice in the control group appeared normal overall, with smooth, shiny fur and continued weight gain. With the exception of the control group, almost all mice fed the alcohol-containing liquid diet experienced varying degrees of weight loss, but the weight loss was more pronounced in the model group (AFLD group). Some mice also exhibited decreased activity and sluggish reactions. The overall mental state and performance of mice in each intervention group improved to varying degrees compared with the model group. The final weight measurement before the end of the experiment showed that mice in the control group weighed significantly more than those in the other four groups (p < 0.05), but there were no significant differences among the four groups (Table 1). Furthermore, Table 1 shows that the liver index of mice in the AFLD group was significantly higher than that in the control group (p < 0.05). The liver index in all three intervention groups was reduced to varying degrees compared with the AFLD group (p < 0.05), with the liver index in the NF group showing a more pronounced decrease compared with the F1-7 group (p < 0.05).

[0039] Table 1 Effects of interventions on body weight and liver indexes of mice (Mean±SD)

[0040] Group Weight (g) Liver index (%) Control <![CDATA[27.74±1.28 b ]]> <![CDATA[4.43±0.26 a ]]> AFLD <![CDATA[22.53±1.30 a ]]> <![CDATA[5.80±0.52 c ]]> NA <![CDATA[23.88±1.38 a ]]> <![CDATA[4.94±0.17 a,b ]]> F1-7 <![CDATA[23.04±1.72 a ]]> <![CDATA[5.21±0.32 b ]]> NF <![CDATA[23.66±1.98 a ]]> <![CDATA[4.62±0.22 a ]]>

[0041] Data marked with different letters are significantly different, p < 0.05.

[0042] Example 3 Detection of serum biochemical indicators

[0043] The mouse blood samples were centrifuged to obtain serum, and the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in serum were determined using an automatic biochemical analyzer.

[0044] The results are as follows Figure 1 Compared with the control group, alcohol intervention increased the level of serum ALT. Compared with the AFLD group, the serum ALT of mice in the NA group, F1-7 group and NF group was significantly reduced. There was no significant difference between the niacin group and the animal Bifidobacterium lactis subspecies F1-7 intervention group. The combined intervention of the two was significantly better than the single intervention of the other two groups, and ALT was reduced by 41% compared with the model group. At the same time, niacin, animal Bifidobacterium lactis subspecies F1-7 and the mixed intervention of the two can improve the abnormal increase of AST level caused by alcohol to varying degrees ( Figure 1 A). Compared with the AFLD group, AST levels in the NA group decreased by 31%, and in the F1-7 group by 20%. The combined intervention of the two groups had the best effect, decreasing by 38%. All three intervention groups were able to effectively improve alcohol-induced liver damage ( Figure 1 B).

[0045] Determination of TG, TC, LDL-C and HDL-C in liver tissue

[0046] Mouse liver tissue was removed from a -80°C freezer. Normal saline was used to rinse the liver tissue surface and remove the fascia. A certain amount of liver tissue was weighed, minced, and placed in normal saline. After thorough homogenization, the mixture was centrifuged at 10,000 rpm for 30 minutes, and the supernatant was retained for later use. TG and TC levels in the supernatant were measured using TC and TG kits from Nanjing Jiancheng Biotechnology Co., Ltd. according to the manufacturer's instructions.

[0047] See the results Figure 2 , the TC level of mice in the AFLD group was significantly increased compared with that in the control group. Probiotics, niacin and the mixed intervention of the two can effectively reduce the TC content in the serum (p<0.05). Compared with the model group, TC in the niacin intervention group decreased by 20%, in the F1-7 group by 21%, and in the NF group by 39%, and the effect was significantly better than that in the other two groups (p<0.05). Compared with the control group, the serum TG of mice in the AFLD group was significantly increased. Both the niacin and probiotic intervention groups can effectively reduce the TG content and reduce it by 18% and 22%, respectively, with no significant difference between the two. The effect of the niacin combined with probiotic intervention group was significantly better than the other two intervention groups, reducing TG by 38%, and there was no significant difference with the control group ( Figure 2 B). Alcohol intervention reduced the HDL-C level in the serum of mice ( Figure 2C), all three intervention groups were able to increase its level, of which the combined intervention group had the best effect, increasing by 42% compared with the model group. The LDL-C level of mice increased significantly after alcohol intervention, and niacin, animal Bifidobacterium lactis subsp. F1-7, and a mixture of the two were able to effectively reduce its content ( Figure 2 D), which were reduced by 31%, 29%, and 40% respectively compared with the model group. Serum indicators indicate that the combined intervention of niacin and probiotics can effectively improve alcohol-induced serum lipid disorders, and the effect is better than the effect of either alone.

[0048] Example 4 Detection of serum inflammatory factors

[0049] The frozen mouse serum was obtained and the levels of endotoxin (LPS), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the serum were detected using enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturer's instructions.

[0050] The results are as follows Figure 3 As shown in Figure 2, alcohol intervention significantly increased the level of LPS in serum, and both niacin and probiotic interventions could effectively improve its level in serum ( Figure 3 A). Compared with the model group, the niacin group decreased by 36%, and the F1-7 intervention group decreased by 37%. The combined intervention effect of the two groups was significantly better than the other two groups (p<0.05), decreasing by 57%. The levels of inflammatory factors were measured. Compared with the control group, the serum inflammatory factor TNF-α level of mice in the alcohol intervention group was significantly increased (p<0.05) ( Figure 3 B). All three intervention groups were able to effectively improve their serum inflammation levels. There was no significant difference between the niacin and probiotic intervention groups. The effect of the niacin combined with animal Bifidobacterium lactis subspecies F1-7 intervention group was better than the other two groups, and was reduced by 66% compared with the model group. Alcohol caused a significant increase in serum IL-6 in mice (p<0.05), which was reduced by 25% by niacin and by 22% by the probiotic intervention group. According to statistical analysis, the effect of the mixed intervention group was significantly better than that of the probiotics alone group (p<0.05), and there was no significant difference with the niacin group. In this study, the change trend of serum IL-1β was basically consistent with that of TNF-α ( Figure 3 D) Both niacin and Bifidobacterium animalis subsp. lactis F1-7 intervention groups effectively reduced serum IL-1β expression in mice, with the combined effect being the most effective. Compared to the model group, IL-1β in the NF group decreased by 59%. The inflammatory responses demonstrated that niacin combined with Bifidobacterium animalis subsp. lactis F1-7 effectively ameliorated the inflammatory response in mice, surpassing either alone.

[0051] Example 5 Histological Analysis and Effects of Nicotinic Acid and Bifidobacterium animalis subsp. lactis F1-7 on Lipid Levels in Mouse Liver

[0052] Mouse liver and small intestinal tissues were fixed with 4% paraformaldehyde and then embedded in paraffin. Paraffin blocks were cut into 5-micron sections, dewaxed in xylene, and then rehydrated with varying degrees of alcohol. Paraffin sections of the liver were stained with hematoxylin and eosin (HE) and oil red solution. Paraffin sections of the small intestine were also stained with HE. Histological changes and fatty degeneration in the liver, as well as morphological changes in the HE sections of the small intestine, were observed under an optical microscope.

[0053] The results are as follows Figure 4 As shown in the figure, compared with the control group, the hepatocytes of the mice in the AFLD group showed diffuse fatty lesions, with more vesicular fatty degeneration of varying sizes, and a large number of inflammatory cells infiltrating the liver lobules. Compared with the AFLD group, the mice in the three intervention groups had significantly reduced fatty lesions in the liver, fewer lipid droplets, and less inflammatory cell infiltration ( Figure 4 A).

[0054] Liver lipid levels were detected, and alcohol intervention significantly increased the TC content in the liver of mice (p < 0.05). Compared with the AFLD group, the TC level in the NA group decreased by 39%, and the TC level in the F1-7 group decreased by 33%, with no significant difference between the two groups. The TC content in the liver of mice in the NF group decreased by 63%, and its effect was relatively better than that of the niacin and probiotics intervention groups ( Figure 4 B). Compared with the control group, the TG level of AFLD mice was significantly increased, while intervention with niacin and Bifidobacterium animalis subsp. lactis F1-7 reduced the TG content in the liver by 36% and 32%, respectively ( Figure 4 C). Compared with the model group, the niacin combined with Bifidobacterium animalis subsp. lactis F1-7 intervention group reduced liver triglyceride by 68%, significantly superior to both the niacin and probiotic intervention groups (p<0.05). This study demonstrated that niacin, Bifidobacterium animalis subsp. lactis F1-7, and their combination were all effective in reducing hepatic lipid accumulation, with the combined intervention being the most effective.

[0055] Example 6 GPR109A protein expression

[0056] The results are as follows Figure 5 As shown, immunofluorescence analysis of GPR109A in the liver revealed that alcohol treatment significantly reduced GPR109A expression in the liver. Compared with the model group, niacin treatment effectively increased GPR109A expression in the liver, with a significant increase in fluorescence intensity (p<0.05). The effect of the probiotic group was not significantly different from that of the niacin group. The combined niacin and probiotic treatment group significantly increased GPR109A content in the liver of mice, and the effect was superior to that of the other two single-treatment groups.

[0057] Example 7 Immunofluorescence (IF) and immunohistochemistry (IHC) staining

[0058] Paraffin-embedded liver and small intestinal tissue blocks were cut into 5-μm sections, dewaxed in xylene, and then rehydrated with graded alcohols. Liver and small intestinal sections were immunofluorescently stained with GPR109A. Small intestinal sections were immunohistochemically stained for intestinal tight junction proteins using the following primary antibodies: ZO-1, occludin, and claudin-1. Observations were made under a light microscope, and images were analyzed using Image J software.

[0059] The results are as follows Figure 6 As shown in Figure 2, compared with the control group, the expression of ZO-1 protein in the model group was significantly downregulated (p<0.05) ( Figure 6 A). Nicotinic acid, Bifidobacterium animalis subsp. lactis F1-7, and their combined intervention can effectively increase the content of ZO-1 in intestinal cells. The content of ZO-1 in the NF group was significantly better than that in the NA and F1-7 groups (p<0.05), and there was no significant difference between the NF group and the control group. The expression of Claudin-1 was observed. Compared with the control group, the positive area of ​​the model group was significantly downregulated, and the expression of Claudin-1 was reduced ( Figure 6 B). The three intervention groups were able to improve its expression to varying degrees, increasing the area of ​​Claudin-1-positive cells in intestinal cells. The combined effect of niacin and probiotics was superior to the effect of either niacin or probiotics alone (p<0.05). Alcohol intervention reduced occludin expression. Compared with the model group, occludin expression in the intestinal tract of mice treated with a combination of niacin and probiotics was significantly increased (p<0.05), with no significant differences among the three intervention groups. Results for key proteins involved in intestinal barrier permeability demonstrated that niacin combined with probiotics effectively improved the intestinal barrier, with a superior effect compared to either niacin or probiotics alone.

[0060] Example 8 Intestinal flora analysis

[0061] like Figure 7 As shown in the figure, analysis of the bacterial community structure at the genus level revealed significant changes in Akkermansia muciniphila (AKK) in the Verrucomicrobia phylum. Compared with the model group, niacin, probiotics, and the mixed group were able to effectively increase the relative abundance of AKK bacteria.

[0062] The various embodiments in this specification are described in a progressive manner, and each embodiment focuses on the differences from other embodiments. The same or similar parts between the various embodiments can be referenced to each other.

[0063] for

[0064] The above description of the disclosed embodiments is intended to enable one skilled in the art to implement or use the present invention. Various modifications to these embodiments will be readily apparent to one skilled in the art, and the general principles defined herein may be implemented in other embodiments without departing from the spirit or scope of the present invention. Therefore, the present invention is not limited to the embodiments shown herein but is intended to conform to the widest scope consistent with the principles and novel features disclosed herein.

Claims

1. Use of niacin in combination with Bifidobacterium lactis subsp. F1-7 in the preparation of a drug for treating and / or preventing alcoholic fatty liver.

2. The use according to claim 1, characterized in that: The combination of niacin and Bifidobacterium lactis subsp. F1-7 improved its intestinal barrier and increased the expression of key barrier proteins ZO-1, Claudin-1 and Occludin.

3. The use according to claim 1, characterized in that: The combination of niacin and Bifidobacterium lactis subsp. F1-7 improved alcohol-induced serum lipid disorders, reduced the TC and TG levels in the serum of mice with alcoholic fatty liver, increased the HDL-C level in the serum of mice, and reduced the LDL-C level.

4. The use according to claim 1, characterized in that: Niacin combined with Bifidobacterium lactis subsp. F1-7 reversed liver damage in mice with alcoholic fatty liver disease and reduced serum ALT and AST levels.

5. The use according to claim 1, characterized in that: The combination of niacin and Bifidobacterium lactis subspecies F1-7 reduces the level of serum inflammatory factors in mice with alcoholic fatty liver; the inflammatory factors are LPS, TNF-α, IL-6, and IL-1β.

6. The use according to claim 1, characterized in that: The combination of niacin and Bifidobacterium lactis subsp. F1-7 improved lipid accumulation in hepatocytes of mice with alcoholic fatty liver and reduced the levels of TC and TD in the liver.

7. A drug for treating and / or preventing alcoholic fatty liver, characterized in that: Includes niacin and Bifidobacterium lactis subsp. F1-7.

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