糖耐康对db/db小鼠肝脏p38MAPK/NF-κBp65信号通路的影响  

Effects of Tang-Nai-Kang on the Liver of db/db Mice via p38MAPK/NF-κBp65 Signaling

作　　者：王明慧 吴丽丽[2] 秦灵灵 吴悠 刘玮 田芃 宋紫临 张程斐[4] 刘铜华[2] Wang Minghui;Wu Lili;Qin Lingling;Wu You;Liu Wei;Tian Peng;Song Zilin;Zhang Chengfei;Liu Tonghua(College of Clinical Medical,Shaanxi University of Chinese Medicine,Xianyang 71200,China;Health-Cultivation Laboratory of the Ministry of Education,Beijing University of Chinese Medicine,Beijing 100029,China;Department of Science and Technology,Beijing University of Chinese Medicine,Beijing 100029,China;Dongfang Hospital,Beijing Uni⁃versity of Chinese Medicine,Beijing 100029,China)

机构地区：[1]陕西中医药大学第一临床医学院,咸阳71200 [2]北京中医药大学教育部中医养生学重点实验室,北京100029 [3]北京中医药大学科技处,北京100029 [4]北京中医药大学东方医院,北京100029

出　　处：《世界科学技术-中医药现代化》2020年第5期1710-1715,共6页Modernization of Traditional Chinese Medicine and Materia Medica-World Science and Technology

基　　金：国家中医药管理局中医药国际合作专项(GZYYGJ2019034):中医药防治慢性病国际合作基地;负责人:刘铜华

摘　　要：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和模型组,每组8只,另设同周龄db/m+小鼠8只为正常组,分别以3.24 g/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、血脂和肝功水平,HE染色观察肝组织病理改变,检测肝组织TNF-α、IL-6、IL-1β含量以及相关蛋白的表达。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,减少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。Objective 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(3.24 g/kg)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-1βand 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.

关 键 词：糖耐康 2型糖尿病 非酒精性脂肪性肝病 DB/DB小鼠 p38MAPK/NF-κBp65信号通路 

分 类 号：R285.5[医药卫生—中药学]