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利用大鼠肾脏缺血再灌注损伤模型,观察了纳洛酮(NAL)对肾缺血再灌注后血中丙二醛(MDA)、超氧化物歧化酶(SOD)及肾组织中Na~+,K~+—ATP酶和Ca~(++)—ATP酶的影响,并观察组织病理学变化。结果显示缺血再灌注后血MDA含量明显升高,SOD活力明显降低,肾组织Na~+,K~+—ATP酶和Ca~(++)—ATP酶活力均显著降低。用NAL(2mg/kg与4mg/kg,ip)后MDA显著下降,SOD和Na~+,K~+—ATP酶和Ca~(++)—ATP酶活力均明显升高。组织病理学检查显示,应用NAL后肾小管上皮细胞的损伤明显减轻。结果提示NAL对肾脏缺血再灌注损伤有一定的保护作用。
The rat model of renal ischemia-reperfusion injury was used to observe the effects of naloxone (NAL) on plasma malondialdehyde (MDA), superoxide dismutase (SOD) and renal Na + , K ~ + -ATPase and Ca ~ (++) - ATPase, and observed histopathological changes. The results showed that the content of blood MDA increased obviously and the activity of SOD decreased significantly after ischemia reperfusion. The activities of Na ~ +, K ~ + -ATPase and Ca ~ (++) - ATPase in kidney decreased significantly. MDA decreased significantly with NAL (2mg / kg and 4mg / kg, ip), SOD and Na ~ +, K ~ + -ATPase and Ca ~ (++) - ATPase activity were significantly increased. Histopathological examination showed that injury of tubular epithelial cells was significantly reduced after NAL application. The results suggest that NAL has a protective effect on renal ischemia-reperfusion injury.