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机构地区:[1]华北石油总医院普外一科,河北任丘062552 [2]河北医科大学解剖学教研室,石家庄050017 [3]河北医科大学临床学院实验中心,石家庄050031
出 处:《解剖学报》2013年第4期550-553,共4页Acta Anatomica Sinica
摘 要:目的观察过氧化物还原酶I-硫氧还蛋白(PrxI-Trx)、超氧化物歧化酶(SOD)及过氧化氢酶(CAT)抗氧化体系在大鼠肝脏缺血再灌注损伤模型中的表达变化,探讨其在抗氧化应激反应中的作用。方法通过无损伤血管夹钳夹通往大鼠肝左叶、肝中叶的血管和胆管蒂,30 min后松开血管夹,制造大鼠70%肝脏缺血再灌注损伤模型。损伤再灌注6h后取血和肝脏。全自动生化分析仪测丙氨酸氨基转移酶(ALT)含量。HE法观察大鼠肝脏形态学改变。采用RT-PCR的方法观察在肝脏缺血再灌注损伤中PrxI-Trx、SOD、CAT氧化还原体系mRNA水平的表达变化。采用Western blotting测定PrxI、SOD和CAT的蛋白表达水平。结果与对照组相比,血清中ALT水平和HE结果均显示肝脏缺血再灌注损伤组大鼠肝细胞明显受损。PrxI-Trx、SOD和CAT的mRNA水平明显升高。同时,PrxI、SOD和CAT的蛋白表达水平也明显升高。结论 PrxI-Trx、SOD和CAT在肝脏缺血再灌注损伤中均发挥了抗氧化应激作用,对肝细胞具有保护作用。Objective To observe the expression change of peroxiredoxin I-thioredoxin (PrxI-Trx), superoxide dismutases (SOD) and catalases (CAT) in hepatic Ischemia-Reperfusion injury of rats, and to explore their role in oxidative-stress response. Methods The hepatic ischemia-reperfusion injury model of rats was established by clipping the hepatic blood vessel released both hepatic left and middle lobes as well as bile duct pedicle with non-damage vascular clamp for 30 minutes. The serum and hepatic tissues were taken 6 hours after clipping. The morphological changes were observed under a microscope using HE staining. The serum alanine aminotransferase(ALT) was detected by Automatic biochemical analyzer. The PrxI-Trx, SOD and CAT mRNA expression were evaluated by RT-PCR. The protein level of PrxI, SOD and CAT were estimated by Western blotting. Results Compared with the control group, the ALT level and HE results of hepatic ischemia-reperfusion injury group showed that liver cells were significantly impaired. The PrxI-Trx, CAT and SOD mRNA expression were increased significantly. The protein level of PrxI, SOD and CAT also increased significantly. Conclusion PrxI-Trx, SOD and CAT may play an important role in inhibiting the oxidative-stress response induced by ischemia-reperfusion injury.
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