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[热毒清对内毒素诱导的实验性家兔弥散性血管内凝血脂质过氧化损伤的肝细胞及线粒体的保护作用]

[Preventive effect of re du qing on hepatocytes and mitochondria damaged by lipid peroxidation in experimental rabbits with endotoxin-induced disseminated intravascular coagulation].

作者信息

Deng Z M, Ye W Y, Li M Z

机构信息

Institute of Integration of TCM and WM, Tanji Medical University, Wuhan.

出版信息

Zhong Xi Yi Jie He Za Zhi. 1991 Feb;11(2):110-1, 70.

PMID:2060052
Abstract

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 less than 0.01), while superoxide dismutase (SOD) activity in hepatic tissue and glutathione peroxidase (GSH-Px) activity in hepatic tissue and mitochondria were decreased significantly (P less than 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 less than 0.01 and P less than 0.05 respectively) compared with the model group. The levels of LPO in the RDQ group did not differ from the control group (P greater than 0.05), but the levels of LPO in the VE group were still higher than those in the control group significantly (P less than 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 less than 0.01). These data suggest that the levels of oxygen free radicals were increased in hepatocytes and mitochondria. This is related to the decreased activities of SOD and GSH-Px in the course of pathogenesis 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.

摘要

本研究以大肠杆菌内毒素诱发家兔全身性施瓦茨曼反应制成弥散性血管内凝血(DIC)模型。实验结果显示,模型组肝组织及线粒体中脂质过氧化物(LPO)水平较对照组显著升高(P<0.01),而肝组织中超氧化物歧化酶(SOD)活性、肝组织及线粒体中谷胱甘肽过氧化物酶(GSH-Px)活性显著降低(P<0.01)。热毒清(RDQ)组和维生素E(VE)组肝组织及线粒体中LPO水平较模型组显著降低(分别为P<0.01和P<0.05)。RDQ组LPO水平与对照组无差异(P>0.05),但VE组LPO水平仍显著高于对照组(P<0.05)。RDQ组和VE组肝组织中SOD活性、肝组织及线粒体中GSH-Px活性也显著高于模型组(P<0.01)。这些数据表明,肝细胞及线粒体中氧自由基水平升高。这与内毒素诱发DIC发病过程中SOD和GSH-Px活性降低有关。本研究提示,脂质过氧化可能是导致肝细胞及线粒体氧化损伤的重要机制之一。

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