目的:基于p38MAPK/NF-κBp65通路，探讨糖耐康对db/db小鼠肝脏的保护作用。方法: 16只 db /db小鼠按体重、血糖随机分为糖耐康组、模型组，每组8只，db/m+小鼠为正常组，分别以 3.24g /kg溶液及等量超纯水灌胃。给药 8周后，检测各组小鼠空腹血糖、血脂、肝功水平，HE染色观察肝组织病理改变，检测肝组织TNF-α、IL-6、IL-1β含量以及相关蛋白。结果: 糖耐康组可显著降低肝重、空腹血糖、血清ALT、AST、TG、TC 和FFA 的水平，下调肝脏组织炎症因子TNF-α、IL-6、IL-1β和p-p38MAPK、核NF-κBp65的蛋白表达水平。病理显示糖耐康组可显著减少小鼠肝细胞的脂肪样变性。结论: 糖耐康可改善db /db 小鼠的糖脂代谢紊乱，降低脂肪在肝脏中的蓄积以及相关炎症因子的表达，其作用机制可能通过调节p38MAPK/NF-κBp65信号通路有关。
aim:This study aimed to explore the impacts of tangnaikang (TNK) on the liver in db/db mice via p38MAPK/NF-κBp65 signaling. METHODS:Sixteen 6-to 8-week-old male db/db mice were divided randomly into the TNK group and the model group with 8 in each group according to their levels of blood glucose and body weight ,while eight db/m+ mice with the same age were made up for the normal group. Mice of the TNK group was administered with (3.24g.kg-1) once a day and the mice of the other groups were treated with Ultra-pure water with the same dosage. After treatment for eight weeks, The fasting blood glucose, blood lipid and liver function of all mice were detected. The pathological changes of liver tissue were observed by HE staining. Comparison of expressions levels of TNF-α,IL-6,IL-1β and certain protein in liver tissue were tested. RESULTS: TNK significantly decreased the levels of the liver weight, the fasting blood glucose, the expression levels of ALT, AST, TG, TC, FFA, the levels of inflammatory factors of TNF-α, IL-6, IL-1βand the protein levels of p-p38MAPK and NF-κBp65 in the liver. Pathology showed that the TNK significantly reduced the steatosis of mouse hepatocytes. CONCLUSION: TNK significantly improves the lipid metabolism, and reduces the accumulation of lipid in the hepatocytes and the levels of inflammatory factors through decreasing the p38MAPK/NF-κBp65 signaling.