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.
摘要：
基于Toll样受体4(TLR4)/髓样分化因子88(MyD88)/核因子κB(NF-κB)信号通路,本研究观察了人参皂苷Rb_1（Rb_1）对db/db肥胖小鼠肝脏脂质代谢的调节作用，并探讨了其可能的机制。将30只6周龄雄性db/db小鼠随机分为模型组,二甲双胍组，和Rb_1组具有低，中等,高剂量,每组6只小鼠。此外,6只年龄匹配的雄性db/m小鼠被分配到正常组.干预持续了五个星期。体重,空腹血糖,每周食物摄入量都是有保证的。实验结束时,检测血脂水平和肝功能。采用苏木精-伊红(HE)染色和油红O染色观察肝组织病理变化。实时定量PCR和石蜡切片免疫组化检测TLR4、MyD88和NF-κBp65的mRNA和蛋白表达。结果:显示与正常组相比,模型组体重显著增加,肝脏重量,肝脏指数,附睾脂肪量,附睾脂肪指数,总胆固醇,低密度脂蛋白胆固醇，肝功能参数，和空腹血糖水平。肝脏脂质积累显著增加，肝脏中TLR4、MyD88和NF-κBp65的mRNA和蛋白表达升高。Rb_1处理后，干预组中的上述参数显示显著逆转.总之,Rb_1可以改善小鼠肥胖和肥胖相关的肝脏脂肪变性，同时调节异常的血脂和葡萄糖代谢。机械上,Rb_1可能通过调节TLR4/MyD88/NF-κB信号通路改善db/db肥胖小鼠肝脏脂肪变性。
