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目的探讨蛇床子素对大鼠肾脏缺血再灌注损伤的保护作用及作用机制。方法将SD大鼠分为假手术组,肾脏缺血再灌注损伤组和蛇床子素预处理组。利用夹闭左侧肾蒂,去除右肾诱导肾脏缺血再灌注损伤模型。观察蛇床子素对肾脏缺血再灌注过程中血清肌酐、尿素氮、活化性半胱天冬酶-9、半胱天冬酶-9、活化性半胱天冬酶-3、半胱天冬酶-3、B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白、胞浆中凋亡诱导因子和细胞色素C的表达水平;线粒体膜电位、氧自由基和三磷酸腺苷酶活性。结果与假手术组相比,肾脏缺血再灌注损伤组血清肌酐、尿素氮、活化性半胱天冬酶-9、半胱天冬酶-9、Bcl-2相关X蛋白、胞浆中凋亡诱导因子、细胞色素C及氧自由基水平明显增加,而线粒体膜电位、三磷酸腺苷酶的活性以及半胱天冬酶-9、活化性半胱天冬酶-3和半胱天冬酶-3的水平明显降低。与肾脏缺血再灌注损伤组相比,蛇床子素组血清肌酐、尿素氮、活化性半胱天冬酶-9、半胱天冬酶-9、Bcl-2相关X蛋白、胞浆中凋亡诱导因子、细胞色素C和氧自由基水平明显降低,而线粒体膜电位、三磷酸腺苷酶活性以及半胱天冬酶-9、活化性半胱天冬酶-3和半胱天冬酶-3的水平明显增高。结论蛇床子素对肾脏缺血再灌注损伤有保护作用,其作用机制可能与其抑制线粒体介导的凋亡途径活性相关。
Objective To investigate the protective effect and mechanism of osthole on renal ischemia-reperfusion injury in rats. Methods SD rats were divided into sham operation group, renal ischemia-reperfusion injury group and osthole pretreatment group. Using the left renal pedicle clamp to remove the right kidney induced renal ischemia-reperfusion injury model. To observe the effects of osthole on serum creatinine, urea nitrogen, active caspase-9, caspase-9, caspase-3, caspase-3 in renal ischemia-reperfusion 3, Bcl-2, Bcl-2 related X protein, the expression of apoptosis-inducing factor and cytochrome C in the cytoplasm; mitochondrial membrane potential, oxygen free radicals and ATPase activity. Results Compared with the sham-operated group, serum creatinine, urea nitrogen, activated caspase-9, caspase-9, Bcl-2 related protein X, Death inducing factor, cytochrome C and oxygen free radicals were significantly increased, while the mitochondrial membrane potential, ATPase activity and caspase-9, caspase-3 and caspase-3 Significantly reduced the level of. Compared with renal ischemia-reperfusion injury group, serum creatinine, urea nitrogen, activated caspase-9, caspase-9, Bcl-2 related X protein, Death inducing factor, cytochrome C and oxygen free radicals were significantly decreased, while mitochondrial membrane potential, ATPase activity, and caspase-9, caspase-3 and caspase-3 Significantly higher levels. Conclusion Osthole can protect renal ischemia-reperfusion injury and its mechanism may be related to its inhibition of mitochondria-mediated apoptotic pathway activity.