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目的:研究丙酮酸乙酯(ethyl pyruvate,EP)对于氯气导致的急性肺损伤(acute lung injury,ALI)和肺组织氧化应激的作用及其机制。方法:30只SD大鼠随机分为阴性对照组、阳性对照组和EP处理组,每组各10只,阴性对照组以空气为对照。阳性对照组和EP处理组给予2 536 mg/m~3的氯气动态染毒,染毒时间为20 min,染毒后立即给予生理盐水或EP(40 mg/kg)处理。染毒6 h后采集样本检测肺组织湿干比、血气、肺组织硫代巴比妥酸反应产物(thiobarbituric acid reactive substances,TBARs)、氧化型谷胱甘肽(glutathione disulfide,GSSG)和还原型谷胱甘肽(glutathione,GSH)含量以及谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-PX)、谷胱甘肽还原酶(glutathione reductase,GR)、总超氧化物歧化酶(total superoxide dismutase,T-SOD)和过氧化氢酶(catalase,CAT)活性。结果:与阴性对照组比较,氯气中毒后肺组织湿干比显著增加,动脉血氧合指数显著降低,肺组织脂质过氧化产物TBARs、GSSG显著增加,GSH含量以及GSH-PX、GR、T-SOD和CAT活性显著降低(P均<0.05)。与阳性对照组比较,EP治疗显著改善了以上指标(P均<0.05)。结论:氯气中毒后引起肺组织氧化应激,造成ALI,EP治疗可以有效减轻氧化应激,缓解急性肺损伤。
Objective: To investigate the effect and mechanism of ethyl pyruvate (EP) on chlorine-induced acute lung injury (ALI) and lung tissue oxidative stress. Methods: Thirty SD rats were randomly divided into negative control group, positive control group and EP treatment group, with 10 rats in each group. Air control group was used as the negative control group. The positive control group and the EP treatment group were given 2 536 mg / m 3 of chlorine dynamic exposure, the exposure time was 20 min, immediately after treatment with saline or EP (40 mg / kg) treatment. Six hours after the exposure, samples were collected to detect the ratio of wet to dry lung tissue, blood gas, lung tissue thiobarbituric acid reactive substances (TBARs), glutathione disulfide (GSSG) and reduced The contents of glutathione (GSH), glutathione peroxidase (GSH-PX), glutathione reductase (GR), total superoxide dismutase, T-SOD) and catalase (CAT) activity. Results: Compared with the negative control group, the lung wet-dry ratio increased significantly, the arterial oxygenation index decreased markedly after the chlorine poisoning. The lung tissue lipid peroxidation products TBARs, GSSG increased significantly, GSH content, GSH-PX, GR, T The activities of SOD and CAT decreased significantly (all P <0.05). Compared with the positive control group, EP treatment significantly improved the above indexes (all P <0.05). Conclusion: Chlorine poisoning causes oxidative stress in lung tissue, resulting in the treatment of ALI and EP can effectively reduce oxidative stress and relieve acute lung injury.