论文部分内容阅读
目的探讨小鼠糖尿病脑损伤时,解偶联蛋白2(UCP2)对下丘脑和海马的作用差异。方法采用长期高脂饮食辅助链脲霉素(STZ)胰岛破坏法建立2型糖尿病小鼠模型,并给予UCP2抑制剂京尼平低剂量(5mg.kg-1.d-1)和高剂量(10mg.kg-1.d-1)连续灌胃2周。比较糖尿病模型小鼠的下丘脑和海马组织中UCP2mRNA、蛋白和能量代谢表达差异。结果与健康对照组小鼠比较。结果与健康小鼠相比,糖尿病模型小鼠下丘脑UCP2表达无明显改变,但海马UCP2mRNA高表达(P<0.05);口服不同剂量的京尼平进行干预,下丘脑和海马UCP2表达呈非线性下降。结论糖尿病模型小鼠的下丘脑和海马存在UCP2表达差异。
Objective To investigate the effect of uncoupling protein 2 (UCP2) on hypothalamus and hippocampus in mice with diabetic brain injury. Methods The model of type 2 diabetic mice was established by long-term high-fat diet assisted by streptozotocin (STZ) islet destroying method. UCP2 inhibitor (5 mg.kg-1.d-1) and high dose 10 mg.kg-1.d-1) for 2 weeks. The differences of UCP2mRNA, protein and energy metabolism in hypothalamus and hippocampus of diabetic mice were compared. Results compared with healthy control mice. Results Compared with healthy mice, the expression of UCP2 in the hypothalamus of diabetic mice showed no significant change, but the expression of UCP2 mRNA in the hippocampus was significantly increased (P <0.05). Compared with healthy mice, UCP2 mRNA expression in the hypothalamus and hippocampus was increased after oral administration of different doses of genipin decline. Conclusion The expression of UCP2 in hypothalamus and hippocampus of diabetic mice is different.