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目的 :通过建立缺血再灌注损伤的动物模型探讨抗氧化能力在缺血预处理对肾脏内源性保护机制中的作用。方法 :54只 SD大鼠随机分为三组 :缺血预处理组、单纯缺血再灌注组和假手术对照组。术后 2 4、72、168小时分三批处死动物、取肾脏组织测定其超氧化物歧化酶 (SOD)、脂质过氧化物 (LPO)和一氧化氮(NO)的含量。结果 :缺血预处理可增加肾组织超氧化物歧化酶 (SOD)合成而减少脂质过氧化物 (LPO)和一氧化氮 (NO)的产生。结论 :抗氧化剂能力可能在缺血预处理对肾脏的内源性保护机制中起重要作用。
OBJECTIVE: To establish an animal model of ischemia-reperfusion injury and to explore the role of antioxidant capacity in renal endogenous protective mechanisms by ischemic preconditioning. Methods: Fifty-four SD rats were randomly divided into three groups: ischemic preconditioning group, ischemia-reperfusion group and sham operation control group. Animals were killed in three batches at 24,72,168 hours after operation. The contents of superoxide dismutase (SOD), lipid peroxides (LPO) and nitric oxide (NO) in the kidneys were measured. Results: Ischemic preconditioning could increase the synthesis of superoxide dismutase (SOD) and decrease the production of lipid peroxides (LPO) and nitric oxide (NO) in renal tissues. CONCLUSIONS: Antioxidant capacity may play an important role in ischemic preconditioning on the renal endogenous protective mechanisms.