激动素对小鼠急性四氯化碳肝损伤的保护作用

目的:探讨激动素对四氯化碳(CCl_4)所致小鼠急性肝损伤的保护作用。方法:建立小鼠四氯化碳急性肝损伤模型,透射电镜观察肝组织超微结构,生化法测定肝组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量与血清丙氨酸转氨酶(ALT)活性、天冬氨酸转氨酶(AST)活性、清蛋白(Alb)含量,观察激动素对肝损伤的保护作用。结果:激动素(20,40 mg·kg~(-1)·d~(-1))能明显抑制肝细胞肿大、空泡变性和染色质增多边集,减轻肝损伤引起的线粒体、粗面内质网肿胀,抑制肝组织中SOD和CAT活性的降低和MDA含量的升高,提高肝组织抗氧化能力;同时激动素能降低血清ALT和AST活性,提高血清AIb含量。结论:激动素能够抵抗CCl_4所致小鼠急性肝损伤,其作用的发挥与清除自由基、提高抗氧化酶活性、维持细胞膜完整性有关。

Protective effects of kinetin on acute liver injury induced by carbon tetrachloride in mice

AIM:To study the protective effects of kinetin on acute liver injury induced by carbon tetrachloride(CC14)in mice.METHODS:The acute liver injury model of mice caused by CCl_4 were established.The ultrastructure of liver was observed under electron microscope.The contents of MDA,the activities of SOD and CAT in the supernates of the mouse liver,and the contents of Alb,the activities of ALT and AST in serum were detected by biochemical method.RESULTS:Volume intumescing,vacuolar degener ation,and nuclear chromatin bordering resulted by CCl_4 was alleviated by ig kinetin(20,40 mg·kg~(-1).d~(-1)), and the swelling of mitochondrion and rough endoplasmic reticulum was ameliorated.Kinetin also significantly inhibited the decrease in activities of SOD,CAT and the increase in content of MDA in liver:inhibited the increase in activities of ALT,AST and the decrease in Alb in serum caused by CCl_4.CONCLUSION:Kinetin can resist acute liver injury in mice induced by CCl_4.The mechanism of its antioxygenic properties may relate to its abilities of eliminating free radical,increasing the activities of antioxidative enzymes,and maintaining completen-ess of cell membrane.