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邓泽明,叶望云,李鸣真.热毒清抗内毒素DIC家兔肝细胞和线粒体过氧化损伤的实验研究[J].,1991,(2):110-111,70
热毒清抗内毒素DIC家兔肝细胞和线粒体过氧化损伤的实验研究
Preventive Effect of Re Du Qing(热毒清)on Hepatocytes and Mitochondria Damaged by Lipid Pcroxidation in Experimental Rabbits with Endotoxin-Induced DIC
  
DOI:
中文关键词:  内毒素  播散性血管内凝血  脂质过氧化物  超氧化物歧化酶  谷胱甘肽过氧化物酶  热毒清
英文关键词:endotoxin  disseminated intravascular coagulation  lipid peroxide  superoxide  dismutase  glutathione peroxidase  Re Du Qing
基金项目:
Author NameAffiliation
Deng Ze-ming 同济医科大学中西医结合研究所 武汉 430030 
Ye Wang-yun 同济医科大学中西医结合研究所 武汉 430030 
Li Ming-zhen 同济医科大学中西医结合研究所 武汉 430030 
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中文摘要:
      本实验采用内毒素所致家兔 DIC 模型,检测肝组织及线粒体脂质过氧化物(LPO)、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)。结果表明模型组 LPO明显升高(P<0.01),SOD 及 GSH-Px 活性明显下降(P<0.01);而热毒清治疗组 LPO 增高不明显(P<0.05),SOD 及 GSH-Px 活性亦不下降(P>0.05)。提示:在内毒素 DIC 时,肝细胞及线粒体对自由基清除功能下降、脂质过氧化损伤较重;而热毒清制剂在内毒素 DIC时,增强了对自由基的清除功能,防止了过氧化损伤,对保护肝细胞和线粒体起到了良好作用。
英文摘要:
      In this study,the general Shwartzman reaction of rabbits induced by Escherichia Coli endotoxin was made as DIC models.The experiments showed that the levels of lipid peroxide(LPO)in hepatic tissue and mitochondria in the model group were increased significantly compared with the control group(P<0.01),while supcroxide dismutase(SOD)activity in hepatic tissue and glutathione perox- idase(GSH-Px)activity in hepatic tissue and mitochondria were decreased significantly(P<0.01), The levels of LPO in hepatic tissue and mitochondria in Re Du Qing(RDQ)group and vitamin E(VE) group were decreased significantly(P<0.01 and P<0.05 respectively)compared with the model group.The levels of LPO in the RDQ group did not differ from the control group(P>0.05),but the levels of LPO in the VE group were still higher than those in the control group significantly(P<0. 05)The SOD activity in hepatic tissue and GSH-Px activity in hepatic tissue and mitochondria in both RDQ group and VE group were also significantly higher than those in the model group(P<0. 01).These data suggest that the levels of oxygen free radicals were increased in hepatocytes and mitochondria.This is related to the decxeased activities of SOD and GSH-Px in the course of pathogcnesis of endotoxin-induced DIC.This study indicates that lipid peroxidation might be one of the important mechanisms resulting in hepatocellular and mitochondria from oxidative damage.
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