CN114164142A - Lactobacillus plantarum Q16 with function of relieving nonalcoholic fatty liver caused by high-fat diet - Google Patents
Lactobacillus plantarum Q16 with function of relieving nonalcoholic fatty liver caused by high-fat diet Download PDFInfo
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- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
- A23L—FOODS, FOODSTUFFS OR NON-ALCOHOLIC BEVERAGES, NOT OTHERWISE PROVIDED FOR; PREPARATION OR TREATMENT THEREOF
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Abstract
The invention provides lactobacillus plantarum Q16 with the function of relieving nonalcoholic fatty liver caused by high-fat diet, which is classified and named as follows: lactobacillus plantarum (lactobacillus plantarum), deposited in the chinese type culture collection at 22 months 10/2021, address: wuhan, Wuhan university zip code: 430072, preservation number is CCTCCNO: M20211311. The strain can effectively reduce the weight of a high-fat diet mouse and the weight of the liver and fat, improve the lipid metabolism in the liver, inhibit the accumulation of triglyceride and improve the energy metabolism in the liver; in addition, the strain also has the capability of optimizing the structure of intestinal flora and has good probiotic function.
Description
One, the technical field
The invention relates to lactobacillus plantarum Q16 with a function of relieving non-alcoholic fatty liver disease caused by high-fat diet, belonging to the field of food microorganisms.
Second, background Art
In the past decades, the number of patients with non-alcoholic fatty liver disease has increased dramatically due to unreasonable dietary structure and lifestyle changes, and has become a serious public health problem worldwide. In addition, the occurrence of non-alcoholic fatty liver disease can induce other diseases such as liver cirrhosis, type ii diabetes, hypertension, cardiovascular diseases, etc., and thus, non-alcoholic fatty liver disease seriously harms human health. A large number of researches show that the occurrence of the non-alcoholic fatty liver disease is related to disorder of intestinal flora structures in a body, and specifically shows that the flora diversity, the symbiotic bacteria ratio and the conditioned pathogen number are reduced.
At present, dietary intervention aiming at the non-alcoholic fatty liver disease mainly comprises ingestion of prebiotics and probiotics, wherein the prebiotics comprise dietary fibers, polyphenols, oligosaccharides and the like, and the prebiotics and the probiotics can improve the intestinal flora structure, so that disorder of the micro-ecosystem is effectively inhibited. However, the mouthfeel of dietary fibers and oligosaccharides, and the absorption and processing techniques of polyphenols have restricted their development. With the growth of the fermentation industry in China, the variety and the number of products containing probiotics are increased, the probiotics can be colonized in human intestinal tracts, have the excellent characteristics of synthesizing essential vitamins, regulating the immune system, improving the intestinal flora structure, relieving the occurrence of metabolic diseases and the like, and are gradually valued and utilized by wide consumers. Therefore, screening of probiotics having the function of inhibiting lipid metabolism disorder is of great significance for development of functional foods.
Third, the invention
Technical problem
The invention aims to provide lactobacillus plantarum capable of relieving the function of nonalcoholic fatty liver caused by high-fat diet.
Technical scheme
The lactobacillus plantarum Q16 has the function of relieving nonalcoholic fatty liver caused by high-fat diet, and the strain Q16 is named in classification: lactobacillus plantarum (Lactobacillus plantarum), deposited in the chinese type culture collection at 22 months 10/2021, address: wuhan, Wuhan university zip code: 430072 with preservation number of CCTCC NO: M20211311.
The application of the lactobacillus plantarum Q16 refers to the application of the lactobacillus plantarum Q16 in relieving nonalcoholic fatty liver caused by high-fat diet. In particular to the application of lactobacillus plantarum Q16 in improving the lipid metabolism in the liver. Or the application of the lactobacillus plantarum Q16 in improving the energy metabolism in the liver. The application of the lactobacillus plantarum Q16 in improving the intestinal flora structure can also be referred to.
Has the advantages that:
(1) the lactobacillus plantarum Q16 provided by the invention obviously improves lipid metabolism and effectively relieves non-alcoholic fatty liver.
(2) The lactobacillus plantarum Q16 provided by the invention effectively improves energy metabolism in the liver and inhibits the accumulation of fat in the liver.
(3) The lactobacillus plantarum Q16 provided by the invention obviously optimizes the intestinal flora structure, thereby improving the intestinal microecosystem.
Animal experiments prove that the lactobacillus plantarum Q16 can effectively reduce the weight of obese mice and reduce the weight of epididymal adipose tissues and livers. Lactobacillus plantarum Q16 reduced mouse body weight, epididymal adipose tissue weight, and liver weight by approximately 14.52%, 26%, and 29.72%, respectively. Apparently, lactobacillus plantarum Q16 was able to inhibit the abnormal accumulation of fat in mice.
Animal experiments prove that the lactobacillus plantarum Q16 can improve lipid metabolism disorder in serum and liver. After the mice take the lactobacillus plantarum Q16, the content of triglyceride, the activity of ALT, the activity of AST and the content of leptin in serum are respectively reduced by 28.40%, 30.35%, 28.98% and 19.33%; the contents of HDL-C and adiponectin in serum are respectively increased by 19.11% and 56.63%; the content of triglyceride and LDL-C in the liver is respectively reduced by 23.60 percent and 20.28 percent; the content of glycerol and acetyl coenzyme A in the liver is respectively increased by 61.15 percent and 100.54 percent. Therefore, the lactobacillus plantarum Q16 can reduce the blood fat of the mice and inhibit the accumulation of fat in the livers of the mice.
Animal experiments prove that the lactobacillus plantarum Q16 promotes lipolysis and fatty acid oxidation in liver, and inhibits lipogenesis and fatty acid de novo synthesis. Western blot analysis results show that after Lactobacillus plantarum Q16 is ingested, the expression level of protein ATGL for regulating lipolysis in mouse liver is increased by about 173.28%; the expression level of protein CPT-1 alpha and PPAR-alpha for regulating fatty acid oxidation is increased by about 86.48% and 152.67%; the expression level of protein DGAT1 for regulating and controlling adipogenesis in the liver is down-regulated by about 20.86 percent; the expression levels of proteins FAS, ACC, SCD-1 and Srebp-1c which regulate the de novo synthesis of fatty acids were reduced by about 29.66%, 32.91%, 43.15% and 23.32%. These results fully demonstrate that lactobacillus plantarum Q16 is capable of directly regulating lipid metabolism-related proteins in the liver, thereby directly alleviating non-alcoholic fatty liver disease.
Animal experiments prove that the lactobacillus plantarum Q16 improves energy metabolism in the liver and promotes energy consumption. The result of Western blot analysis shows that the expression levels of PGC-1 alpha, p-AMPK alpha and FGF21 in mouse liver are respectively improved by 169.58%, 75.72% and 117.61% after the lactobacillus plantarum Q16 is ingested. Lactobacillus plantarum Q16 promotes energy expenditure, thereby indirectly inhibiting the accumulation of lipids in the liver.
Animal experiments prove that the lactobacillus plantarum Q16 can effectively increase the diversity of intestinal flora and the abundance of symbiotic bacteria, and simultaneously reduce the proportion of conditional pathogenic bacteria. Intestinal microbial sequencing results show that after lactobacillus plantarum Q16 is ingested, the relative abundance of conditional pathogenic bacteria proteobacteria, Desulfuromicrobiaceae, Desulfurvibrio, helicobacter and Mucispiralium in the colon of a mouse is respectively reduced by 72.67%, 83.12%, 84.88%, 85.34% and 81.88%; the symbiotic flora S24-7, the Lactobacillus family, the Lactobacillus and the Parabacteroides are respectively improved by 124.14%, 315.03%, 118.68% and 263.62%. These results indicate that lactobacillus plantarum Q16 inhibits the occurrence of intestinal inflammation, improves the intestinal micro-ecological environment, and then indirectly relieves non-alcoholic fatty liver by reducing the abundance of conditional pathogenic bacteria, promoting the proliferation of commensal flora.
Fourthly, explanation of the attached drawings:
FIG. 1 is a phylogenetic tree of Lactobacillus plantarum Q16;
FIG. 2 shows the body weight, liver weight and epididymal adipose tissue weight of each group of mice;
FIG. 3 is a graph showing the serum levels of triglycerides, leptin, adiponectin, total cholesterol, glutamic-pyruvic transaminase, glutamic-oxaloacetic transaminase, high density lipoprotein cholesterol, low density lipoprotein cholesterol, tumor lethal factor-alpha, and interleukin-1 beta in each group of mice;
FIG. 4 shows the amounts of triglyceride, total cholesterol, HDL cholesterol, LDL cholesterol, glycerol and acetyl-CoA in the livers of various groups of mice;
FIG. 5 is a photograph of H & E and oil red stained sections of livers of various groups of mice;
FIG. 6 shows the expression levels of proteins involved in lipid metabolism in the livers of mice in each group;
FIG. 7 shows the expression levels of energy metabolism-related proteins in the livers of mice in each group;
FIG. 8 is an analysis of the diversity of the flora Alpha in the colon of each group of mice;
FIG. 9 is an analysis of the intestinal flora at the phylum level in each group of mice;
FIG. 10 is an analysis of intestinal flora at the family level for each group of mice;
FIG. 11 is an analysis of the intestinal flora at the genus level in each group of mice.
Biological preservation
Lactobacillus plantarum Q16, the strain being classified under the name: lactobacillus plantarum (Lactobacillus plantarum), deposited in the chinese type culture collection at 22 months 10/2021, address: wuhan, Wuhan university zip code: 430072, preservation number is CCTCC NO: M20211311.
Fifth, detailed description of the invention
The invention is further illustrated by specific embodiments and with reference to the accompanying drawings:
1. identification and culture of lactobacillus plantarum Q16
Transporting the yoghourt self-made by Qinghai herdsmen to a laboratory at low temperature, mixing the yoghourt sample with the sterile MRS according to the volume ratio of 1:100 under the aseptic condition, and enriching the lactic acid bacteria. Uniformly coating the cultured flora in an MRS solid culture medium, picking a single colony for culturing again, carrying out streak culture on the cultured bacteria, picking the single colony again, continuing to expand and cultivate, repeating the steps for 3 times, picking the single colony, and carrying out sequencing identification. A single colony was identified as Lactobacillus plantarum, which we named Lactobacillus plantarum Q16 (FIG. 1).
2. Preparation of Lactobacillus plantarum Q16 bacterial suspension
The cultured Lactobacillus plantarum Q16 was centrifuged (8000 rpm, 10 minutes), the supernatant was discarded, washed three times with 0.1mol/L sterilized PBS buffer (pH 7.2), and the concentration of Lactobacillus plantarum Q16 was adjusted to 10 using this buffer9cfu/mL。
3. Effect of Lactobacillus plantarum Q16 on mouse body weight and organs
Animal experiments 4-week-old mice of a specific pathogen-free grade (purchased from the university of Yangzhou, comparative medicine center) were used, and after one week of acclimation, normal group (NC group) mice were fed with normal diet, and model group (HFD group) and sample group (PL group) mice were fed with high-fat diet. According to the method of Dang et al (Dang et al, Food funct.,2018,9, 3630-3639), the mice in the sample group were gavaged 10 days9Lactobacillus plantarum Q16 of cfu, both normal and model groupsThe mice were gavaged with an equal volume of sterile normal saline for 8 weeks, the weight of the mice was recorded, and the weight of the liver and epididymal fat was measured, all measurements being in eight replicates. As shown in FIG. 2, after the Lactobacillus plantarum Q16 was ingested, the body weight of the mice was reduced from 50.88 + -2.88 g to 43.50 + -3.46 g, the liver weight was reduced from 2.32 + -0.41 g to 1.63 + -0.17 g, and the epididymis adipose tissue weight was reduced from 1.55 + -0.37 g to 1.15 + -0.25 g, compared to the high fat model group.
4. Effect of Lactobacillus plantarum Q16 on parameters related to lipid metabolism in mouse serum
The method of Zhu et al (Zhu et al, Food funct.,2018,9, 3509-. The kit is used for measuring the content of triglyceride, leptin, adiponectin, glutamic pyruvic transaminase (ALT), glutamic oxaloacetic transaminase (AST), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) in serum (all the kits are purchased from Nanjing BioLimited), and the results are shown in figure 3. compared with the mice of a high-fat model group, after the Lactobacillus plantarum Q16 is ingested, the concentration of triglyceride in the serum of the mice is reduced to 6.96 +/-1.41 mmol/L, the ALT activity is reduced to 14.63 +/-2.17U/L from 21.01 +/-4.19U/L, the AST activity is reduced to 55.89 +/-3.22U/L from 78.69 +/-10.75U/L, the concentration of HDL-C is reduced to 3.96 +/-0.53 mmol/L from 3.20 +/-0.57 mmol/L, and the leptin concentration is reduced to 3.96 +/-0.53 mmol/L from 3.89 ng/0.53 ng/L, the concentration of the adiponectin rises from 8.57 +/-2.02 mg/L to 19.76 +/-4.58 mg/L. The concentrations of total cholesterol and LDL-C in serum did not change significantly. Therefore, lactobacillus plantarum Q16 was effective in improving lipid metabolism in serum of mice with a high fat diet.
5. Effect of Lactobacillus plantarum Q16 on parameters related to lipid metabolism in mouse liver
According to the method of Gao et al (Gao et al, Food funct.,2021,12, 373-386), after the liver of the mouse is removed, 100mg of liver sample is accurately weighed into a sterile centrifuge tube, 1ml of sterile PBS buffer (0.1mol/L, pH 7.2) is added, homogenized by an automatic homogenizer until no obvious block is formed, then centrifuged at 4 ℃ and 2000 rpm for 10 minutes, and the supernatant is sucked into another sterile centrifuge tube and stored at 4 ℃ for later use. The levels of triglyceride, HDL-C, LDL-C, total cholesterol, glycerol, and acetyl-CoA in the liver homogenate supernatant were measured using a kit, and the protein content in the liver homogenate supernatant was measured using BCA (kit available from Shanghai Biyunnan Bio Inc.) for calibration of parameters. As shown in FIG. 4, after the intake of Lactobacillus plantarum Q16, the triglyceride concentration in the liver of mice decreased from 22.12. + -. 3.65mmol/mg prot to 16.90. + -. 3.42mmol/mg prot, the LDL-C concentration decreased from 4.28. + -. 0.55mmol/mg prot to 3.41. + -. 0.55mmol/mg prot, the glycerol concentration increased from 32.57. + -. 10.53mmol/mg prot to 52.48. + -. 5.07mmol/mg prot, the acetyl-CoA concentration increased from 1.02. + -. 0.44pmol/μ g prot to 2.04. + -. 0.25pmol/μ g prot, and the total cholesterol and HDL-C concentration in the liver did not change significantly, compared with the mice in the high fat model group. Therefore, the lactobacillus plantarum Q16 can obviously reduce the content of triglyceride and LDL-C in the liver, increase the content of glycerol and acetyl coenzyme A and effectively inhibit the accumulation of fat in the liver.
6. Effect of Lactobacillus plantarum Q16 on mouse liver architecture
Referring to Wang et al (Wang et al, j. funct. foods,2020,68,103923), 400 mg of fresh mouse liver was accurately weighed, washed with sterile saline and placed in a sterile centrifuge tube, 1ml of 4% paraformaldehyde was added for tissue fixation, and stored at 4 degrees for later use. Then, all tissues were dehydrated, embedded in paraffin, sectioned with a microtome, stained with hematoxylin, eosin, and oil red, respectively, and the microstructure of the tissues was observed with a microscope.
As shown in FIG. 5, the liver of the mouse in the high-fat model group had a large number of lipid droplets, and the results of oil red staining showed that the liver had a large amount of lipids; in contrast, mice administered lactobacillus plantarum Q16 showed no significant lipid droplet cells in the liver and a significant reduction in lipids.
7. Effect of Lactobacillus plantarum Q16 on lipid metabolism in the liver of mice
In order to explore the lipid metabolism regulation mechanism of lactobacillus plantarum Q16, the invention measures the expression level of some proteins related to lipid metabolism.
Referring to Xia et al (Xia et al, biomed. Pharmacother.,2019,118,109287), 100mg of liver sample was accurately weighed, placed in 1ml of a lysate (containing protease and phosphatase inhibitors) of Shanghai Biyun Bio Inc., and three small magnetic beads, the tissue sample was thoroughly disrupted by a homogenizer, centrifuged at 12000g for 20min at 4 ℃ to obtain the supernatant as total protein of the tissue, the supernatant was taken into another centrifuge tube, and the protein concentration was determined by a BCA kit (purchased from Shanghai Biyun Bio Inc.). 6-15% of separation gel and concentrated gel are prepared, and proper separation gel concentration is selected according to the molecular weight of the target protein. Mixing protein extract and protein sample buffer solution, heating in 100 deg.C boiling water for 8min, centrifuging at 10000g for 1min, adding the mixture into protein gel pore groove (ensuring total amount of each pore protein to be 50 μ g), adding rainbow Marker (purchased from Nanjing Nuojingzhan biological Co., Ltd.) into each gel via a hole, running at 90V constant pressure for 30min, separating strips on the rainbow Marker, changing to 120V constant pressure, and running to the bottom of separation gel from the Marker. The protein gel was removed, the gel near the target protein was cut with a scalpel, the protein was transferred with an NC membrane (available from GE Healthcare Life Science, USA), and the membrane was placed in a buffer for membrane transfer and then transferred at a constant current of 400mA for 20min (the target protein is less than 150 kDa). Then the NC membrane was placed in a blocking solution (TBST + 5% skimmed milk powder) and blocked for 2 hours, after blocking, the NC membrane was placed in a diluted primary antibody solution (CPT-1. alpha., PPAR. alpha., Srebp-1c, ACC, SCD-1, ATGL, DGAT1 and FGF21 primary antibodies were obtained from Affinity Biosciences, Inc., in Heizhou, FAS primary antibodies were obtained from Cell Signaling Technology, Inc., in U.S.A.; GAPDH, PGC-1. alpha., SIRT1, p-AMPK. alpha., AMPK. and NRF1 primary antibodies were obtained from Shanghai Biyun Biosciences, Inc.) and the NC membrane was fully contacted with the antibody by ice-bath for 12 hours on a decolorization shaker. After incubation, the unbound antibody on the membrane was washed with membrane washing solution (TBST + 1% skim milk powder) three times for 8min each, and then the NC membrane was incubated with diluted secondary antibody (purchased from Strobilekusho bioengineering, Inc. of Wuhan Dynasty) at room temperature for 2h, and then washed with membrane washing solution three times for 8min each. ECL luminescence solution (available from Affinity Biosciences, Inc., Chang.) was dropped on the membrane by a pipette, the membrane was gently shaken to bring the luminescence solution into sufficient contact with the membrane surface, exposure was taken in an ECL chemiluminescence apparatus, and the optical density of the band was quantitatively analyzed by Image J software.
As shown in FIG. 6, the expression levels of Fatty Acid Synthase (FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA desaturase-1 (SCD-1), sterol regulatory element-binding protein-1 c (Srebp-1c), and diacylglycerol-acyltransferase 1(DGAT1) in the liver of mice were decreased by 0.39, 0.43, 0.60, 0.40, and 0.36 fold, respectively, after the intake of Lactobacillus plantarum Q16, as compared to the mice in the high-fat model group; the expression levels of carnitine palmitate transferase-1 alpha (CPT-1 alpha), peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and fatty triglyceride lipase (ATGL) in the liver are respectively improved by 0.36, 0.51 and 0.70 times, and the results fully indicate that the lactobacillus plantarum Q16 can directly regulate the protein related to lipid metabolism in the liver so as to relieve the nonalcoholic fatty liver.
8. Effect of Lactobacillus plantarum Q16 on energy metabolism-related proteins in mouse liver
In order to explore the mechanism of the lactobacillus plantarum Q16 for regulating energy metabolism, the invention measures the expression level of some proteins related to energy metabolism.
And 7, determining the energy metabolism related protein in the liver by using the conditions of extracting the protein and Western blot in the liver.
As shown in fig. 7, the expression levels of peroxisome proliferator-activated receptor- γ coactivator-1 α (PGC-1 α), phosphorylated AMP-dependent protein kinase α (p-AMPK α), and fibroblast growth factor 21(FGF21) in the liver of the mouse were increased by 0.79, 0.62, and 0.62 times, respectively, as compared to the mice in the high fat model group, after ingestion of lactobacillus plantarum Q16. The lactobacillus plantarum Q16 is shown to indirectly inhibit the accumulation of lipid in the liver by activating FGF21/Adiponectin/AMPK alpha/PGC-1 alpha pathway, thereby enhancing the mitochondrial biosynthesis, improving the energy metabolism in the liver and promoting the energy consumption.
9. Regulation of intestinal flora structure by lactobacillus plantarum Q16
In order to explore the influence of lactobacillus plantarum Q16 on the structure of intestinal flora, the structure of intestinal flora in the colon of a mouse is determined by taking colon contents as a research object and utilizing a metagenomic sequencing technology.
Referring to the method of Li et al (Li et al, Food Res. int.,2021,143,110270), 200mg of mouse feces were quickly weighed into a sterilized 2mL centrifuge tube, crushed, homogenized, placed on ice, and feces genomic DNA extraction kit (from Biochemical technology, Inc., Beijing Tiangen) was performed as follows: adding 1.4mL of buffer GSL into a fecal sample, shaking for 1min, uniformly mixing the sample, incubating for 10min at 70 ℃, vortexing for 15s, centrifuging for 1min at 12000 Xg, transferring supernatant into a new sterilized centrifuge tube, adding an inhibitor adsorption sheet into the centrifuge tube, shaking until the adsorption sheet is completely dissolved, standing for 1min at room temperature, centrifuging for 3min at 12000 Xg, sucking supernatant into a new centrifuge tube, centrifuging for 3min at 12000 Xg, sucking 200 mu L of supernatant into another centrifuge tube, adding 15 mu L of protease K, adding 200 mu L of buffer GB, vortexing for 15s at shaking, incubating for 10min at 70 ℃, adding 200 mu L of absolute ethyl alcohol, vortexing and uniformly mixing, adding mixed solution into an adsorption column, collecting by using a sleeve, purifying DNA by using buffer GD and rinsing solution PW respectively, collecting DNA by using buffer TB, and storing in a refrigerator at-20 ℃. The purity and concentration of DNA were measured by Nanodrop as to OD260/OD280 and concentration, and the ratio of OD to OD of about 1.8 indicated that the purity of DNA was good. Then amplifying the V3-V4 region of the 16S rRNA of the bacteria by adopting primers of a forward primer 338F (5'-ACTCCTACGGGAGGCAGCA-3') and a reverse primer 806R (5 '-GGACTACHVGGGTWTCTAAT-3'), wherein the PCR reaction system is as follows: mu.L of each of 1. mu.L of LDNA template, 0.25. mu. L Q5 DNA polymerase, 5 Xreaction buffer and 5 Xhigh GC buffer, 1. mu.L of 10. mu.M forward and reverse primers, 0.5. mu.L of 10mM dNTP, 11.25. mu.L of ddH2And O. The PCR reaction conditions are as follows: pre-denaturation at 98 ℃ for 30s, 25 cycles of denaturation at 98 ℃ for 15s, annealing at 56 ℃ for 30s and elongation at 72 ℃ for 30s, and mostThen renaturation is carried out for 5min at 72 ℃, and the amplified product is purified and sequenced. Because the number of sequences obtained by high-throughput sequencing is huge, original data needs to be filtered and screened to remove chimera sequences, so that the accuracy of the data can be improved, the working efficiency is improved, in addition, for the convenience of subsequent analysis, the sequences also need to be clustered, and clustering with the sequence similarity of more than or equal to 97 percent is usually carried out, namely a classification Unit (OTU) can be operated. On the basis of OTU division, Alpha diversity analysis can be further carried out to determine the abundance of communities in the sample, the composition of the flora in the sample can be further determined through different taxonomic levels, and Beta diversity analysis can explain the difference of the flora among sample groups.
The overall structure of intestinal flora of each group is shown in figure 8, and compared with mice in a high-fat model group, lactobacillus plantarum Q16 improves the Chano 1 index, Shannon index and Simpson index by about 0.57 times, 0.08 times and 0.01 times respectively, which shows that lactobacillus plantarum Q16 improves the richness and diversity of intestinal flora of the mice.
In addition, differences in flora at the phylum, family and genus level were also evident. As shown in fig. 9-11, lactobacillus plantarum Q16 inhibited the proliferation of harmful flora, such as proteobacteria, vibrionaceae, rikenaceae, oscillatoria, cladosporium, devulcanium, helicobacter, allorhabdus and Mucispirillum, at phylum, family and genus level, as compared to mice of the high-fat model group; and significantly increases the abundance of the probiotic groups bacteroidetes, S24-7, lactobacillaceae, lactobacillus and parabacteroides. On one hand, proteobacteria, vibrionaceae, vibrio, helicobacter and Mucispirillum are the main conditional pathogens for causing intestinal inflammation, and the pathogens cause the translocation of lipid and endotoxin in the intestinal tract into a circulating system by causing the intestinal inflammation and further damaging the intestinal barrier so as to cause the systemic inflammation and the accumulation of the lipid; on the other hand, S24-7, Lactobacillus and Parabacteroids can reduce the pH value in the intestinal tract by producing organic acid, improve the intestinal tract micro-ecosystem and effectively enhance the intestinal tract barrier, and in addition, short chain fatty acid produced by the bacteria can enter the liver through enterohepatic circulation, so that the activity of AMPK is improved, the generation of fatty acid oxidation reaction in the liver is promoted, and the abnormal accumulation of lipid in the liver is inhibited.
In conclusion, the lactobacillus plantarum Q16 relieves the non-alcoholic fatty liver caused by high-fat diet through three ways of regulating the protein of lipid metabolism, the protein of energy metabolism and the intestinal flora structure, and has good probiotic effect.
Sequence listing
<110> Nanjing university of agriculture
<120> Lactobacillus plantarum Q16 having function of alleviating non-alcoholic fatty liver disease caused by high-fat diet
<160> 2
<170> SIPOSequenceListing 1.0
<210> 1
<211> 19
<212> DNA
<213> Artificial Sequence (Artificial Sequence)
<400> 1
actcctacgg gaggcagca 19
<210> 2
<211> 20
<212> DNA
<213> Artificial Sequence (Artificial Sequence)
<400> 2
Claims (6)
1. Lactobacillus plantarum Q16 having the function of relieving nonalcoholic fatty liver caused by high-fat diet, the strain Q16 is named after classification: lactobacillus plantarum (lactobacillus plantarum), deposited in the chinese type culture collection at 22 months 10/2021, address: wuhan, Wuhan university zip code: 430072 with preservation number of CCTCC NO: M20211311.
2. The use of lactobacillus plantarum Q16, according to claim 1.
3. The use of claim 2, wherein the Lactobacillus plantarum Q16 is used for relieving non-alcoholic fatty liver disease caused by high-fat diet.
4. The use according to claim 2 or 3, which is the use of Lactobacillus plantarum Q16 for improving lipid metabolism in the liver.
5. The use according to claim 2 or 3, which is the use of Lactobacillus plantarum Q16 for improving energy metabolism in the liver.
6. The use according to claim 2 or 3, wherein the Lactobacillus plantarum Q16 is used for improving the intestinal flora structure.
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