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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。
In this experiment, rabbit models of DIC induced by endotoxin were used to detect liver tissue and mitochondrial lipid peroxide (LPO), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The results showed that the LPO in the model group was significantly increased (P<0.01), and the activity of SOD and GSH-Px was significantly decreased (P<0.01). However, the LPO in the heat-toxin-treated group was not significantly increased (P<0.05). SOD and GSH-Px activity It did not decrease (P>0.05). Tip: When endotoxin DIC, hepatocyte and mitochondria have a reduced function of free radical scavenging and heavier lipid peroxidation; while the hot toxin formulation enhances the free radical scavenging function and has prevented Oxidative damage plays a good role in protecting hepatocytes and mitochondria.