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目的观察大鼠肝缺血再灌注损伤时阿托伐他汀钙与缺血后处理对其保护效应的比较,并探讨其作用机制。方法 28只健康雄性SD大鼠随机分成假手术组(CON)、缺血再灌注组(IR)、缺血后处理组(IP0)、阿托伐他汀钙预处理组(APC),每组7只。建立大鼠70%的在体肝脏缺血再灌注模型,各组于最后灌注后经肝上下腔静脉取血,用于检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST);取肝匀浆低温离心后采用试剂盒测定肝组织中总超氧化物歧化酶(TSOD)、丙二醛(MDA)、髓过氧化物酶(MPO)、一氧化氮(NO)、一氧化氮合酶(NOS)含量变化;同时取肝脏组织作病理切片观察。结果动物模型经持续45min缺血及90min再灌注后,肝功能明显受损,抗氧化酶活力显著下降,肝组织大片坏死;缺血后处理组和阿托伐他汀钙组能明显改善肝IR损伤程度,升高SOD活性,降低MDA、MPO和体内NO的水平,明显减轻肝窦上皮和血管内皮的损伤,减轻肝细胞损伤和炎性细胞的浸润。结论缺血后处理组和阿托伐他汀钙预处理组对大鼠肝缺血再灌注损伤有保护作用且效果相当,而药物处理更简便。其可能的机制为提高机体抗氧化能力、清除氧自由基和抗炎作用有关。
Objective To observe the protective effect of atorvastatin calcium and ischemic postconditioning on hepatic ischemia-reperfusion injury in rats and its mechanism of action. Methods Twenty-eight healthy male Sprague-Dawley rats were randomly divided into sham operation group (CON), ischemia / reperfusion group (IP0), atorvastatin calcium preconditioning group (APC) only. The model of ischemia-reperfusion in vivo liver was established in 70% of the rats. Blood was drawn from the superior and inferior vena cava after the last perfusion in each group to detect serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) The contents of total superoxide dismutase (TSOD), malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO), nitric oxide synthase ) Content changes; at the same time take the liver tissue for pathological observation. Results After the rats were subjected to ischemia for 45 min and reperfusion 90 min, the liver function was significantly impaired and the activity of antioxidant enzymes was significantly decreased. The liver tissue was necrosis. The ischemic postconditioning group and atorvastatin calcium group significantly improved the liver IR injury Level, increase SOD activity, reduce the level of MDA, MPO and NO in the body, significantly reduce the sinusoidal epithelium and vascular endothelial damage, reduce the damage of liver cells and infiltration of inflammatory cells. Conclusion The ischemic postconditioning group and the atorvastatin calcium preconditioning group have a protective effect on hepatic ischemia-reperfusion injury in rats and their effects are similar, but the drug treatment is more convenient. Its possible mechanism is to improve the body’s antioxidant capacity, scavenging oxygen free radicals and anti-inflammatory effects.