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Effects of Ozone Oxidative Preconditioning on TNF-α Release 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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摘要

Ozone oxidative preconditioning is a prophylactic approach, which favors 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 serum TNF-α levels and as a modulator of oxidative stress on hepatic tissue in endotoxic shock model (mice treated with lipopolysaccharide (LPS)). Ozone/oxygen gaseous mixture which was administered intraperitoneally (0.2, 0.4, and 1.2 mg/kg) once daily for five days before LPS (0.1 mg/kg, intraperitoneal). TNF-α was 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-α levels in mouse serum. Ozone/oxygen gaseous mixture reduced serum TNF-α levels ina dose-dependent manner. Statistically significant decreases inTNF-α levels after LPS injection were observed in micepretreated with ozone intraperitoneal applications at 0.2(78%), 0.4 (98%), and 1.2 (99%). Also a significantincrease in TBARS content was observed in the hepatic tissue ofLPS-treated mice, whereas enzymatic activity of glutathion-Stransferase and glutathione peroxidase was decreased. However inozone-treated animals a significant decrease in TBARS content wasappreciated as well as an increase in the activity of antioxidantenzymes. These results indicate that ozone oxidativepreconditioning exerts inhibitory effects on TNF-αproduction and on the other hand it exerts influence on theantioxidant-prooxidant balance for preservation of cell redoxstate 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,并作为肝组织氧化应激的调节剂。臭氧/氧气混合气体,在LPS(0.1μg/ kg,腹膜内)之前,每天一次腹膜内给予(0.2、0.4和1.2μmg/ kg),持续5天。通过对L-929细胞的细胞毒性测量TNF-α。测量了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/氧气混合气体可降低体内的血清TNF-α水平剂量依赖性的方式。统计上显着减少小鼠注射LPS后的TNF-α水平臭氧腹膜内应用0.2预处理(78%),0.4(98%)和1.2(99%)。也很重要在肝组织中观察到TBARS含量增加。LPS处理的小鼠,而谷胱甘肽-S的酶活性转移酶和谷胱甘肽过氧化物酶降低。但是在臭氧处理的动物的TBARS含量显着下降,赞赏以及抗氧化剂活性的增加酶。这些结果表明,臭氧具有氧化性预处理对TNF-α产生抑制作用生产,另一方面,它对抗氧化剂-抗氧化剂平衡,可保护细胞氧化还原通过增加内源性抗氧化系统状态。

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