详细信息

鲨鱼肝蛋白粗提物对大鼠肝线粒体抗氧化功能的影响  ( EI收录)  

Effects of Shark Protein Crude Extract Administration on Liver Mitochondrial Antioxidant Defenses in Rats

文献类型:期刊文献

中文题名:鲨鱼肝蛋白粗提物对大鼠肝线粒体抗氧化功能的影响

英文题名:Effects of Shark Protein Crude Extract Administration on Liver Mitochondrial Antioxidant Defenses in Rats

作者:范秋领[1];黄才国[2];金艳[2];缪辉南[2];焦炳华[2];袁勤生[1]

机构:[1]华东理工大学生物反应器工程国家重点实验室,上海200237;[2]第二军医大学基础医学部生物化学与分子生物学教研室,上海200433

年份:2005

卷号:31

期号:5

起止页码:598

中文期刊名:华东理工大学学报(自然科学版)

外文期刊名:Journal of East China University of Science and Technology

收录:CSTPCD;;EI(收录号:2005479497643);Scopus;北大核心:【北大核心2004】;CSCD:【CSCD2011_2012】;

基金:上海-SK研究与发展基金(2003003-S)

语种:中文

中文关键词:鲨鱼肝蛋白粗提物;硫代乙酰胺;急性肝损伤;线粒体;呼吸功能;抗氧化

外文关键词:shark protein extract; thioacetamide, acute liver injury; mitochondria; respiratory function; antioxidant defenses

摘要:以400 m g/kg 2次腹腔注射硫代乙酰胺(TAA)建立大鼠急性肝损伤模型,并在注射TAA前1 h以80 m g/kg 2次腹腔注射鲨鱼肝蛋白粗提物进行预防,研究了鲨鱼肝蛋白粗提物对大鼠肝线粒体抗氧化功能的影响。注射TAA后,大鼠肝脏线粒体腺苷二磷酸(ADP)诱导的氧消耗、呼吸控制率(RCR)、磷/氧比(P/O)、氧化磷酸化率均低于对照组,而预防组线粒体ADP诱导的氧消耗、呼吸控制率、P/O和氧化磷酸化效率均高于模型组;TAA降低了线粒体中谷胱甘肽、谷胱甘肽还原酶、谷胱甘肽过氧化物酶的水平,而鲨鱼肝蛋白粗提物则使线粒体中谷胱甘肽过氧化物酶和超氧化物歧化酶的水平明显升高,说明鲨鱼肝蛋白粗提物能部分修复线粒体受损的呼吸功能,增强线粒体抗氧化能力。
The effects of shark protein crude extract administration on liver mitochondrial antioxidant defenses were investigated in rats. Rats were given two consecutive intraperitoneal injections of thioacetamide (TAA, 400 mg/kg body weight) and shark protein extract (80 mg/kg body weight) 1 h before TAA treatment with a 24 h interval in model and therapy groups respectively. TAA administration decreased the ADP stimulated oxygen consumption, respiratory control ratio (RCR), the P/O value and oxidative phosphorylation ratio in isolated mitochondria, but shark protein extract could suppressed the effect of TAA. TAA administration decreased the levels of glutathione, glutathione peroxidase, glutathione reductase in mitochondria, and shark protein extract administration increased the levels of glutathione peroxidase and superoxide dismutase. These illustrated that shark protein extract could partially repair mitochondrial respiratory function impaired by TAA administration, and increase mitochondrial antioxidant defenses.

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