昆仑雪菊原花青素对四氯化碳致小鼠肝损伤的保护作用

本文研究了昆仑雪菊原花青素(KCPC)对四氯化碳(CCl4)致小鼠急性肝损伤的保护作用。采用CCl4建立肝损伤模型,观察KCPC对肝损伤小鼠肝脏病理变化和肝脏指数等的影响;检测小鼠丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量;采用Fe2+-Vc诱导线粒体细胞膜肿胀,分析KCPC对抑制线粒体肿胀的作用,并检测琥珀酸脱氢酶(SDH)活性。结果表明,KCPC中剂量组及高剂量组绝大部分肝组织结构正常,而模型组的小鼠肝组织出现病变坏死,而且血清中ALT、AST显著上升(p0.01)。此外,KCPC高剂量组(800 mg/kg)的ALT、AST活性分别比模型组降低了82.46%和69.41%,且SOD、GSH-Px活性分别增加了101.08%和92.13%(p0.01),MDA含量降低了45.16%(p0.01)。KCPC还具有一定抑制线粒体肿胀的能力,且400mg/kg剂量组的SDH活性为模型组的1.22倍。上述结果表明,KCPC对CCl4诱导的小鼠肝损伤具有保护作用,其机制可能与提高抗氧化酶的活性有关。

Protection of Liver Injury Induced by Carbon Tetrachloride of Kunlun Chrysanthemun by Proanthocyanidon

The protective effect of Kunlun chrysanthemun proanthocyanidin (KCPC) against acute liver injury induced by carbon tetrachloride in mice was investigated. The effects of KCPC on liver appearance pathology and liver index in mice with acute liver injury were analyzed; alanine aminotransferase (ALT) and aspartate aminotransferase (AST) level in serum, as well as antioxidant enzymes SOD, GSH-Px and lipid peroxidase MDA activities in liver of mice were determined by biochemical methods. In addition, the protective effect of KCPC on mitochondria was analyzed by inhibiting mitochondrial membrane swelling induced by Fe2+-Vc and the activity of succinic dehydrogenase (SDH) was evaluated. The results showed that, in the KCPC groups, no distinct pathological changes occurred, while for the control group, the pathology of mice liver tissue dramatically changed, with the activity of ALT and AST in serum increasing remarkably. The activity of ALT and AST in the high-dose KCPC group (800 mg/kg) decreased by 82.5% and 69.4%, respectively. The activities of SOD and GSH-Px increased by 101.1% and 92.1%% (p<0.01), respectively, whereas the MDA content decreased 45.2% (p<0.01). In addition, KCPC has the ability to inhibit the swelling of mitochondria, and the activity of SDH in 400 mg/kg dose group was 1.22 times that of the control group. The results suggest that KCPC exerts a significant protective effect on CCl4 induced liver injury in mice, and its mechanism may be related to the upregulation of antioxidative enzyme activity.