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本文探讨SMAO休克时大鼠肝线粒体损伤以及自由基清除酶(剂)对肝线粒体的保护作用。实验组线粒体RCR于松夹1 hr即明显下降(P<0.05),松夹2 hr下降更甚(P<0.01)。ADP/O值也明显降低(P<0.05)。单用ALLO或伍用SOD+CAT,SOD+ALLO,SOD+CAT+ALLO治疗对SMAO休克大鼠肝线粒体氧化磷酸化功能均有显著的保护作用,并且在松夹2 hr后,除单用ALLO组外,其它诸组RCR仍较对照组无显著下降(P>0.05),而且还明显高于实验组(P<0.01),其中以SOD+CAT+ALLO伍用效果最佳。提示脂质过氧化损伤是SMAO休克时肝脏线粒体损伤的重要原因;而伍用自由基清除酶(剂)是防止其损伤的理想选择。
This article investigates the protective effects of mitochondria and hepatic mitochondria induced by free radical scavenging enzymes in rats with SMAO shock. In the experimental group, mitochondrial RCR decreased significantly (P <0.05) at 1 hr and at 2 hr (P <0.01). ADP / O values were also significantly lower (P <0.05). Treatment with SMA alone or ALLO with SOD + CAT, SOD + ALLO and SOD + CAT + ALLO all significantly protected the mitochondrial oxidative phosphorylation of SMAO-treated rats, (P> 0.05), but also significantly higher than the experimental group (P <0.01). Among them, SOD + CAT + ALLO was the best. It is suggested that lipid peroxidation injury is an important cause of liver mitochondrial damage during SMAO shock. However, the use of free radical scavenging enzyme (Agent) is an ideal choice to prevent its damage.