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本研究采用家兔内毒素休克模型,实验分为四组:对照组;内毒素血症组;磷酸氯喹(CQ)预处理组;地塞米松(DXM)预处理组,测定血浆和肝、肾、心、肺线粒体PLA_2活性及线粒体膜流动性。结果表明正常对照和注射内毒素(ET)后1、3、5、8h血浆PLA_2分别为15.52±5.31与25.83±7.86、30.54±11.53、37.13±8.53、41.88±7.32U/ml,注射ET后血浆PLA_2显著高于注射前(P<0.05)。CQ、DXM预处理组则血浆PLA_2显著低于内毒素血症动物(P<0.05)。注射ET8h后肝、肾、心、肺线粒体PLA_2活性显著高于正常对照组。而CQ、DXM预处理组显著低于内毒素血症组(P<0.05)。同时内毒素血症组肝、肾、心、肺线粒体膜流动性降低,分子排列有序性升高,膜脂区微粘度升高;而CQ、DXM预处理组肝、肾、心、肺线粒体膜流动性显著改善。线粒体PLA_2升高和膜流动性降低呈显著正相关。
In this study, rabbit endotoxin shock model was used. The experiment was divided into four groups: control group, endotoxemia group, CQ pretreatment group and DXM preconditioning group. Plasma and liver and kidney , Heart, lung mitochondrial PLA 2 activity and mitochondrial membrane fluidity. The results showed that the levels of plasma PLA_2 were 15.52 ± 5.31 and 25.83 ± 7.86, 30.54 ± 11.53, 37.13 ± 8.53 and 41.88 ± 7.32 U / ml respectively at 1, 3, 5 and 8h after injection of endotoxin (ET) PLA 2 was significantly higher than before injection (P <0.05). In CQ and DXM preconditioning groups, plasma PLA 2 was significantly lower than that in endotoxemia animals (P <0.05). After ET8h injection, the activity of mitochondrial PLA2 in liver, kidney, heart and lung was significantly higher than that in normal control group. The CQ, DXM pretreatment group was significantly lower than the endotoxemia group (P <0.05). In the endotoxemia group, the fluidity of mitochondrial membrane of liver, kidney, heart and lung decreased, the order of molecular arrangement increased and the microviscosity of membrane lipid region increased. However, the mitochondria of liver, kidney, heart and lung in CQ and DXM preconditioning group Membrane fluidity is significantly improved. There was a significant positive correlation between the increase of mitochondrial PLA 2 and the decrease of membrane fluidity.