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目的建立实验性2型糖尿病(T2DM)鼠模型并探讨脑组织和血管病变与脑组织及血液中醛糖还原酶(AR)活性、超氧阴离子(O2—.)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)活性改变及其在T2DM发生发展中的相互关系。方法组织切片观察脑组织和微血管病理改变;紫外分光光度法及化学比色法检测血清O2—.、GSH-PX、SOD、CAT活性;NADPH减少法测定脑组织和血清AR活性。结果实验性T2DM鼠脑微血管和脑组织病理形态学改变明显;脑组织和血清AR活性显著高于正常对照组(P<0.05);O2—.活力显著高于正常对照组(P<0.05)、SOD、GSH-Px活性显著低于正常对照组(P<0.05);T2DM鼠H组SOD活性显著低于L组(P<0.05)。结论实验性T2DM鼠脑组织出现病理变化与血液和脑组织中氧化与抗氧化物质异常改变密切相关,在诸多因素中,SOD活性降低可能是起主导作用的因素。
Objective To establish a murine model of experimental type 2 diabetes mellitus (T2DM) and investigate the relationship between brain tissue and vascular lesions and the activities of aldose reductase (AR), superoxide anion (O2-), superoxide dismutase (SOD) ), Catalase (CAT), glutathione peroxidase (GSH-PX) activity and their relationship in the occurrence and development of T2DM. Methods Tissue sections were used to observe the pathological changes of brain tissue and microvessels. The levels of O2 -, GSH-PX, SOD and CAT were detected by UV spectrophotometry and chemical colorimetry. The activities of AR and AR were measured by NADPH reduction assay. Results The histopathological changes of cerebral microvessels and brain tissues in experimental T2DM rats were obvious. The activity of AR in brain tissue and serum was significantly higher than that in normal control group (P <0.05). The activity of O2- in brain tissue and serum was significantly higher than that in normal control group (P <0.05) The activities of SOD and GSH-Px were significantly lower than those of normal control group (P <0.05). The activity of SOD in H group was significantly lower than that in L group (P <0.05). Conclusion The pathological changes in brain tissue of T2DM rats are closely related to the abnormal changes of oxidation and antioxidants in blood and brain tissue. Among many factors, the decrease of SOD activity may play a leading role.