摘要
目的:观察高血糖对正常或伴随炎症、纤维化肝的氧化还原状态的影响。方法:将24只大鼠分为对照组、高血糖组、正常血糖+四氯化碳组、高血糖+四氯化碳组(STZ诱导高血糖,4周后用四氯化碳诱导肝纤维化),第9周处死。测量其肝组织GSH、SOD、MDA的水平。结果:未注射CCl4加高血糖组肝MDA较对照组有所增加,GSH、SOD则有一定程度的减少。CCl4组和CCl4加糖尿病组的MAD明显升高,GSH、SOD则降低,它们之间无明显差异。结论:8周的高血糖可能一定程度的改变肝脏的氧化还原状态,但这种改变不够明显。在并发肝脏炎症时,高血糖不能进一步加重肝脏的氧化打击。
Objective:To investigate ff hyperglycemia can affect the redox homeostasis in the inflammatory and fibrotic liver of rat induced by carbon tetrachloride (CCl4).Methods:Normal male Sprague-Dawley rats were randomly divided into four groups:control group (n=6),hyperglycemia group (n=5),normal blood glucose plus CCl4group (n=6),hyperglycemia plus CCl4group (n=5).[hyperglycemia induced with STZ(60 mg/kg);liver inflammation and fibrosis induced by CCl4(40%,2 ml/kg,biw)after hyperglycemia for four weeks.]All the rats were killed at week 9.GSH.SOD.MDA of the liver were measured. Results:The hyperglycemia group had higher level of MDA and lower levels of GSH,SOD compared with control group,but there was no statistic significance between them.The CCl4 group and hyperglycemia plus CCl4 group had an increased level of MDA and deceased level of GSH.SOD in liver compared with control group or hyperglycemia group. Conclusion:Hyperglycemia for 8 weeks can change the redox homeostasis in liver,but can not aggravate the oxidative injury in inflammatory or fibrotic liver.
出处
《现代医药卫生》
2005年第20期2725-2726,共2页
Journal of Modern Medicine & Health
关键词
高血糖
四氯化碳
氧化还原状态
Hyperglycemia
Carbon tetrachloride
Redox homeostasis