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目的:探讨2型糖尿病肝损害的发生及可能的发病机制。方法:KKAy糖尿病小鼠高脂饮食喂养,28周后处死小鼠,分别取血清和肝组织,全自动生化法检测血糖(GLU)、甘油三酯(TG)、总胆固醇(TC)、谷丙转氨酶(ALT)、谷草转氨酶(AST)等生化指标;HE、Masson染色观察肝组织病理形态学改变;TUNNEL法检测肝细胞凋亡变化;放免法检测肝组织中IL-1β、TNF-α含量的变化等。结果:与正常小鼠相比,KKAy糖尿病小鼠血清中GLU、TG、TC均增高(P<0.01),血清中ALT、AST增高(P<0.01),肝组织病理形态学检测可见肝细胞呈脂肪变性,肝组织纤维化,并可见肝细胞凋亡;肝组织中IL-1β、TNF-α含量明显增高(P<0.01)。结论:糖尿病KKAy小鼠存在肝损害;IL-1β、TNF-α可能是其损伤机制之一。
Objective: To investigate the occurrence and possible pathogenesis of type 2 diabetic liver damage. Methods: KKAy diabetic mice were fed with high-fat diet. After 28 weeks, mice were killed and serum and liver tissues were taken out. The levels of blood glucose (GLU), triglyceride (TG), total cholesterol (TC) (ALT), aspartate aminotransferase (AST) and other biochemical indicators; HE, Masson staining liver histopathological changes; TUNNEL method to detect changes in hepatocyte apoptosis; RIA to detect the content of IL-1β, TNF- Change and so on. Results: Compared with normal mice, the serum levels of GLU, TG and TC in KKAy diabetic mice increased (P <0.01) and the levels of ALT and AST in serum increased (P <0.01). The pathological changes of hepatic cells Steatosis and hepatic fibrosis, and showed hepatocyte apoptosis. The levels of IL-1β and TNF-α in liver tissue were significantly increased (P <0.01). Conclusion: KKAy diabetic mice have liver damage. IL-1β and TNF-α may be one of the mechanisms of their injury.