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Comparative Neuroprotective Effects of Dexamethasone and Minocycline during Hepatic Encephalopathy

机译:地塞米松和米诺环素在肝性脑病中的比较神经保护作用

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Objective.Encephalopathy and brain edema are serious complications of acute liver injury and may lead to rapid death of patients. The present study was designed to investigate the role of the inflammatory mediators and oxidative stress in the cytotoxic brain oedema and the neuroprotective effects of both minocycline and dexamethasone.Methods.48 male albino rats were divided into 4 groups: control group, acute liver injury (ALI) group, minocycline pretreated ALI group, and dexamethasone pretreated ALI group. 24 hours after acute liver injury serum ammonia, liver enzymes, brain levels of heme oxygenase-1 gene, iNOS gene expression, nitriteitrate, and cytokines were measured. In addition, the grades of encephalopathy and brain water content were assessed.Results.ALI was associated with significant increases in all measured inflammatory mediators, oxidative stress, iNOS gene expression, and nitriteitrate. Both minocycline and dexamethasone significantly modulated the inflammatory changes and the oxidativeitrosative stress associated with ALI. However, only minocycline but not dexamethasone significantly reduced the cytotoxic brain oedema.Conclusion.Both minocycline and dexamethasone could modulate inflammatory and oxidative changes observed in brain after ALI and could be novel preventative therapy for hepatic encephalopathy episodes.
机译:目的:脑病和脑水肿是急性肝损伤的严重并发症,可能导致患者快速死亡。本研究旨在探讨炎症介质和氧化应激在细胞毒性脑水肿中的作用以及米诺环素和地塞米松的神经保护作用。方法。48只雄性白化病大鼠分为4组:对照组,急性肝损伤( ALI)组,米诺环素预处理ALI组和地塞米松预处理ALI组。急性肝损伤后24小时,测定血清氨,肝酶,脑血红素加氧酶-1基因,iNOS基因表达,亚硝酸盐/硝酸盐和细胞因子。此外,还评估了脑病的等级和脑含水量。结果:ALI与所有测得的炎症介质,氧化应激,iNOS基因表达以及亚硝酸盐/硝酸盐的显着增加有关。米诺环素和地塞米松均显着调节与ALI相关的炎症变化和氧化/亚硝化应激。然而,仅米诺环素而不是地塞米松能显着降低细胞毒性脑水肿。结论:米诺环素和地塞米松均可以调节ALI后脑部的炎症和氧化变化,是预防肝性脑病发作的新方法。

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