人参皂苷Rb1通过抑制JNK信号通路改善糖尿病大鼠肝脏糖脂代谢异常

Ginsenoside Rb1 ameliorates abnormal glucolipid metabolism of liver through inhibition of JNK signal pathway in diabetic rats

目的:探索人参皂苷Rb1对糖尿病大鼠肝脏糖脂代谢的影响及其调控机制。方法:链脲佐菌素(Streptozotocin,STZ)处理建立糖尿病大鼠模型。HE染色观察肝脏病变。TUNEL染色检测肝细胞凋亡情况。血糖仪检测血糖浓度。放射免疫分析检测胰岛素和C肽水平。运用全自动化分析仪测定总胆固醇、三酰甘油、低密度脂蛋白胆固醇和高密度脂蛋白胆固醇浓度。蛋白印迹检测JNK信号通路相关蛋白JNK1、c-Jun表达。免疫组化分析炎症因子IL-6、IL-1β和TNF-α蛋白表达。结果:人参皂苷Rb1可改善糖尿病大鼠肝损伤。与健康对照组相比,STZ诱导组的血糖浓度明显升高,胰岛素及C肽浓度明显降低(P<0.05)。与STZ诱导组相比,STZ+人参皂苷Rb1组的血糖浓度明显降低,胰岛素及C肽浓度明显升高(P<0.05)。与健康对照组相比,STZ诱导组的总胆固醇、三酰甘油、低密度脂蛋白胆固醇升高,高密度脂蛋白胆固醇降低(P<0.05)。与STZ诱导组相比,STZ+人参皂苷Rb1组总胆固醇、三酰甘油、低密度脂蛋白胆固醇降低,高密度脂蛋白胆固醇升高(P<0.05)。STZ诱导组JNK1和c-Jun蛋白相对表达量明显高于健康对照组(P<0.05)。STZ+人参皂苷Rb1组JNK1和c-Jun蛋白相对表达量明显低于STZ诱导组(P<0.05)。与健康对照组相比,STZ诱导组的IL-6、IL-1β和TNF-α表达明显升高。STZ+人参皂苷Rb1组IL-6、IL-1β和TNF-α表达明显低于STZ诱导组。结论:人参皂苷Rb1可通过JNK信号通路改善糖尿病大鼠肝损伤及糖脂代谢异常,降低炎症反应。

Objective:To explore effects and mechanism on glucolipid metabolism of liver of ginsenoside Rb1 in diabetic rats.Methods:Diabetic rat model was induced by streptozotocin(STZ).Hepatic pathological changes were observed by hematoxylin-eosin(HE)staining.Apoptosis was analyzed through Terminal deoxynucleotidyl transferase-mediated dUTP nick labeling(TUNEL)staining.Blood glucose was determined with glucometer.The level of insulin and C peptide was tested by radioimmunoassay.Total cholesterol,low density lipoprotein cholesterol,high-density lipoprotein cholesterol,triglyceride was detected by full automatic biochemical analyzer.The expression of JNK signal pathway related proteins JNK1 and c-Jun was measured by Western blot.The expression of inflammatory factor IL-6,IL-1βand TNF-αwas detected by immunohistochemistry.Results:Liver injury was ameliorated by ginsenoside Rb1 in diabetic rats.Compared with control group,the level of blood glucose in STZ-induced diabetic rat group was increased with attenuated level of insulin and C peptide(P<0.05).Compared with STZ-induced diabetic rat group,the level of blood glucose in STZ+ginsenoside Rb1 group was decreased with enhancive level of insulin and C peptide(P<0.05).Compared with control group,the level of total cholesterol,triglyceride and low density lipoprotein cholesterol in STZ-induced diabetic rat group was elevated with attenuated level of high-density lipoprotein cholesterol(P<0.05).Compared with STZ-induced diabetic rat group,the level of total cholesterol,triglyceride and low density lipoprotein cholesterol in STZ+ginsenoside Rb1 group declined with elevated level of high-density lipoprotein cholesterol(P<0.05).The relative expression of JNK1 and c-Jun in STZ-induced diabetic rat group was higher than control group(P<0.05).The relative expression of JNK1 and c-Jun in STZ+ginsenoside Rb1 group was lower than STZ-induced diabetic rat group(P<0.05).Compared with control group,the expression of IL-6,IL-1βand TNF-αin STZ-induced diabetic rat group was enhanced(P<0.05).The expression of IL-6,IL-1βand TNF-αin STZ+ginsenoside Rb1 group was lower than STZ-induced diabetic rat group(P<0.05).Conclusion:Ginsenoside Rb1 ameliorates liver injury,abnormal glucolipid metabolism and inflammatory response of liver through inhibition of JNK signal pathway in diabetic rats.