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首页> 外文期刊>Mediators of inflammation >Effects of Ozone Oxidative Preconditioning on TNF-αRelease and Antioxidant-Prooxidant Intracellular Balance in Mice During Endotoxic Shock
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Effects of Ozone Oxidative Preconditioning on TNF-αRelease and Antioxidant-Prooxidant Intracellular Balance in Mice During Endotoxic Shock

机译:臭氧氧化预处理对内毒素性休克小鼠TNF-α释放及抗氧化-抗氧化剂细胞内平衡的影响

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Ozone oxidative preconditioning is a prophylactic approach, whichfavors the antioxidant-prooxidant balance for preservation of cell redox state by the increase of antioxidant endogenous systems in both in vivo and in vitro experimental models. Our aim is to analyze the effect of ozone oxidative preconditioning on serumTNF-αlevels and as a modulator of oxidative stress on hepatic tissue in entodoxic shock model (mice treated with lipopolysaccharide (LPS)). Ozone/oxygen gaseous mixture which was administered intraperitoneally (0.2,0.4, and1.2mg/kg) once daily for five days before LPS (0.1mg/kg, intraperitoneal). TNF-αwas measured by cytotoxicity on L-929 cells. Biochemical parameters such as thiobarbituric acid reactive substances (TBARS), enzymatic activity of catalase,glutathione peroxidase, and glutathione-S transferase were measured in hepatic tissue. One hour after LPS injection there was a significant increase in TNF-αlevels in mouse serum. Ozone/oxygen gaseous mixture reduced serum TNF-αlevels in a dose-dependent manner. Statistically significant decreases inTNF-αlevels after LPS injection were observed in mice pretreated with ozone intraperitoneal applications at0.2(78%),0.4(98%), and1.2(99%). Also a significant increase in TBARS content was observed in the hepatic tissue of LPS-treated mice, whereas enzymatic activity of glutathion-Stransferase and glutathione peroxidase was decreased. However in ozone-treated animals a significant decrease in TBARS content was appreciated as well as an increase in the activity of antioxidant enzymes. These results indicate that ozone oxidative preconditioning exerts inhibitory effects on TNF-αproduction and on the other hand it exerts influence on the antioxidant-prooxidant balance for preservation of cell redox state by the increase of endogenous antioxidant systems.
机译:臭氧氧化预处理是一种预防性方法,通过体内和体外实验模型中抗氧化剂内源性系统的增加,有利于抗氧化剂-促氧化剂平衡以保持细胞氧化还原状态。我们的目的是分析内毒素休克模型(用脂多糖(LPS)治疗的小鼠)中臭氧氧化预处理对血清TNF-α水平的影响以及作为肝组织氧化应激的调节剂。在LPS(0.1mg / kg,腹膜内)之前,每天一次腹膜内施用(0.2、0.4和1.2mg / kg)的臭氧/氧气混合物,持续五天。通过对L-929细胞的细胞毒性测量TNF-α。测量肝组织中的生化参数,如硫代巴比妥酸反应性物质(TBARS),过氧化氢酶,谷胱甘肽过氧化物酶和谷胱甘肽S转移酶的酶活性。 LPS注射后一小时,小鼠血清中的TNF-α水平显着增加。臭氧/氧气混合气体以剂量依赖性方式降低血清TNF-α水平。在经腹膜内臭氧处理的小鼠中,经LPS注射后,TNF-α水平有统计学显着降低,分别为0.2(78%),0.4(98%)和1.2(99%)。在LPS处理的小鼠的肝组织中,还观察到TBARS含量的显着增加,而谷胱甘肽-S转移酶和谷胱甘肽过氧化物酶的酶活性降低。然而,在用臭氧处理的动物中,TBARS含量的显着降低以及抗氧化酶活性的提高是令人赞赏的。这些结果表明,臭氧氧化预处理对TNF-α的产生具有抑制作用,另一方面,它通过增加内源性抗氧化剂体系而对抗氧化剂-抗氧化剂平衡产生影响,以保持细胞的氧化还原状态。

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