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[Intervention mechanism of ginsenoside Rb_1 on liver steatosis in db/db obese mice based on TLR4/MyD88/NF-κB
Ting-Ting Li1, Cheng-Fei Zhang1, Xiang-Yu Guo1
1Dongfang Hospital of Beijing University of Chinese Medicine Beijing 100078, China.
Abstract:
Based on the Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor kappaB(NF-κB) signaling pathway, this study observed the regulatory effect of ginsenoside Rb_1(Rb_1) on liver lipid metabolism in db/db obese mice and explored its potential mechanism. Thirty 6-week-old male db/db mice were randomly divided into a model group, a metformin group, and Rb_1 groups with low, medium, and high doses, with six mice in each group. Additionally, six age-matched male db/m mice were assigned to the normal group. The intervention lasted for five weeks. Body weight, fasting blood glucose, and food intake were mea-sured weekly. At the end of the experiment, serum lipid levels and liver function were detected. Hematoxylin-eosin(HE) staining and oil red O staining were performed to observe pathological changes in liver tissue. Real-time quantitative PCR and immunohistochemistry on paraffin sections were used to detect the mRNA and protein expression of TLR4, MyD88, and NF-κB p65. RESULTS:: showed that compared with the normal group, the model group exhibited significant increases in body weight, liver weight, liver index, epididymal fat mass, epididymal fat index, total cholesterol, low-density lipoprotein cholesterol, liver function parameters, and fasting blood glucose levels. Liver lipid accumulation significantly increased, along with elevated mRNA and protein expression of TLR4, MyD88, and NF-κB p65 in the liver. After Rb_1 treatment, the above-mentioned parameters in the intervention groups showed significant reversals. In conclusion, Rb_1 can improve obesity and obesity-related hepatic steatosis in mice while regulating abnormal lipid and glucose meta-bolism. Mechanistically, Rb_1 may improve liver steatosis in db/db obese mice by modulating the TLR4/MyD88/NF-κB signaling pathway.
Insights
Ginsenoside Rb_1 improves obesity and liver steatosis in mice by regulating lipid and glucose metabolism via the Toll-like receptor 4/myeloid differentiation factor 88/nuclear factor kappaB pathway.
Area of Science:
- Pharmacology and Toxicology
- Metabolic Diseases
- Molecular Biology
Context:
- Obesity and associated hepatic steatosis are significant health concerns.
- The Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor kappaB (NF-κB) pathway is implicated in metabolic dysregulation.
- Ginsenoside Rb_1 is a compound with potential therapeutic properties.
Purpose:
- To investigate the effect of ginsenoside Rb_1 (Rb_1) on liver lipid metabolism in diet-induced obese mice.
- To explore the underlying mechanism involving the TLR4/MyD88/NF-κB signaling pathway.
Summary:
- Obese db/db mice treated with Rb_1 showed significant improvements in body weight, liver parameters, lipid profiles, and glucose levels compared to controls.
- Rb_1 treatment reversed diet-induced increases in liver lipid accumulation and normalized the expression of TLR4, MyD88, and NF-κB p65.
- These findings indicate Rb_1's efficacy in ameliorating obesity-related hepatic steatosis and metabolic dysfunction.
Impact:
- Ginsenoside Rb_1 demonstrates therapeutic potential for managing obesity and non-alcoholic fatty liver disease.
- Modulating the TLR4/MyD88/NF-κB pathway offers a novel therapeutic strategy for metabolic disorders.
- This study provides mechanistic insights into the anti-obesity and anti-steatosis effects of ginsenosides.
