Masted Bifidobacteria V9 reduces liver fatty degeneration and aminoization in rats.

.Non-alcoholic fatty liver disease (NAFLD) as a chronic liver disease, mainly in the liver without alcohol consumption of fat deposition or degeneration phenomenon, in fat deposition, oxidative stress and chronic inflammation of the liver, NAFLD may develop into non-alcoholic fatty hepatitis (NASH), may also develop cirrhosis. A high-fat diet and lack of exercise are the main causes of NAFLD, lifestyle changes and weight loss can alleviate NAFLD, while a growing body of research has shown that gut microbes can participate in the metabolism of related factors in the liver; Therefore, this experiment established a high-fat diet (HFD) rat model to explore the mitigating effect of Bifidobacteria V9 on NAFLD.Experimental Design The experimental details 1. The subjects selected 40 healthy rats as experimental materials for a four-week experiment, randomly divided into five groups: control group, HFD group, HFD-Berberine group, V9 treatment group (HFD/V9) and V9 control group (CON/V9), each group of 8 rats.. 2. Experimental methodIn addition to the control group and the V9 control group, rats in other groups were given a high-fat diet, while rats in the V9 treatment group and V9 control group were given a lactobacillus Bifidobacteria V9 gastric filling (1x
10
9
CFU); and the HD-Berberine group was given a small pyridine (300mg/kg).. 3. The test methodblood samples from rats and liver tissue samples after the end of the test.Note:Control Group HFD Group (HFD): High-fat Diet HFD-Berberine Group: High-Fat Diet and Small Sepline V9 Treatment Group (HFD/V9): High-Fat Diet and C.D. Bifidobacteria V9 VV 9 Control Group (CON/V9): Results of the C. D. V9 The reduction ofHFD-induced liver damage In order to explore the mitigation effect of HFD V9 on HFD, the development of liver injury was detected at histological level by sumu-I-red staining. It was found that after a high-fat diet of up to 6 weeks, there was significant damage to liver tissue, small leaf structure disorders, hypertrophobic cells, and severe fat degeneration (a large number of lipid droplet formation). In contrast, the treatment of C. D. V9 and nicotine significantly improved the structure of the small leaves of the liver to reduce liver fatty degeneration (Figure 1a). Compared to the HFD group, both LDF V9 and chlorpyridine therapy significantly reduced levels of alanine transaminase (ALT) and acetone transaminase (AST) in serum (Figure 1b, c). This suggests that Bifidobacteria V9 can reduce liver damage and fat degeneration caused by a high-fat diet.
. Figure 1: a is a slice of liver tissue after HE staining; b is ALT level; c is AST level 2. Improved HDD-induced lipid and glucose metabolic disorders HFD group triglyceride (TG) and free fatty acid (FFA) levels increased, while the V9 treatment group and HFD-Berberine group have lower TG and FFA levels (Figure 2a, b). In addition, the treatment of C. D.D. V9 and chlorpyridine can reduce the levels of HFD-induced hepatic glycogen (Figure 2c). Compared to the HFD group, supplementation with Bifidobacteria V9 can also significantly reduce total cholesterol (TC) and icing sugar levels on an empty stomach (Figure 2d). This suggests that lactobacillus Bifidobacteria V9 can improve the metabolic disorders of lipids and glucose.. Figure 2: a is triglyceride (TG) level; b is free fatty acid (FFA) level; c is hepatic glycogen level; d is fasting blood sugar level 3. Reversing imbalances involving genes associated with lipid and glucose metabolismAn evaluation of key signaling paths found that HFD induced an increase in mRNA expression of protein 1c (SREBP-1c) and fatty acid synthase (FAS) in rat-induced steroid regulators, which were subsequently reduced by treatment of C.D. V9 and chlorophylline (Figure 3a, b). The mRNA expression of PPAR-ɑ in the liver was significantly reduced by HFD attack and recovered through C.D. V9 treatment, while the level of pyridine treatment did not change significantly. Compared to the control group, the MRNA expression of PPAR-ɑ the V9 control group increased (Figure 3c). After protein imprinting analysis, the expression of phosphatization AMPK can be restored by ceding Bifidobacteria V9 and chlorpyridine treatment (Figure 3d).. Figure 3: a is the mRNA expression details of SREBP-1c, b is the mRNA expression details of FAS, c is the mRNA expression details of PPAR-ɑ in the liver, and d is the protein imprinting analysis 4 Reducing the primary response induced by HFDexplores the anti-inflammatory effects of C.D. V9 and measures the levels of mRNA in the liver and serum TNF-alpha, IL-1 beta and IL-6. Compared to the control group, HFD stimulation led to significant increases in serum TNF-alpha, IL-1 beta and IL-6 levels, as did the mRNA expression of these cytokines. The expression of HFD-induced mRNA and related proteins can be significantly inhibited by C. Bifidobacteria V9, and a similar trend has been found in small pyridine (Figure 4a-f). This suggests that both Bifidobacteria V9 and nicotine can reduce HFD-induced levels of inflammatory cytokines.. Figure 4: Details of mRNA expression of related inflammatory cytokines 5. Inhibition of expression of TLR and NLRP3As shown in Figures 5a and b, mRNA expression in the HFD group of TLR4 and TLR9 increased significantly compared to the control group, while LFD V9 and chlorpyridoline decreased their expression. Significant decreases in mRNA expression of NLRP3 and ASC were also found in the V9 treatment group and the HFD-Berberine group (Figure 5c, d). . Figure 5: Effects of C.D. V9 on liver TLRs, NLRP3, and ASC Inhibit AMPK, AKT, and NF-B activation To further evaluate the HPLD-induced NAFLD protection mechanism of C.D. V9, continue to evaluate downstream signal path changes mediated by TLR. HFD induction can lead to increased phosphateation of JNK, ERK and AKT, while CLF V9 and cytobacterium can reduce their activation. MilkYlobacteria V9 can also inhibit NF-B phosphorylation. This suggests that the activation of C.D. V9 inhibits AMPK, AKT, and NF-B will contribute to anti-inflammatory effects. Conclusion Milk Bifidobacteria V9 can reduce liver fat degeneration and aminoation in non-alcoholic fatty liver rats, as well as liver tissue damage induced by a high-fat diet, and fat degeneration. Regulates related metabolism and improves lipid levels and glucose content. At the same time, it was found that Bifidobacteria V9 also had significant anti-inflammatory effect, reducing the expression of cell inflammatory factors. Improves NAFLD by suppressing AMPK, TLR, and NF-B signal paths to inhibit amino transfer.
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