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首页> 外文期刊>Journal of pharmacology & toxicology. >A Preliminary Study of Dexamethasone Against Ischemia/Reperfusion Liver Injury in Rats
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A Preliminary Study of Dexamethasone Against Ischemia/Reperfusion Liver Injury in Rats

机译:地塞米松对大鼠缺血/再灌注肝损伤的初步研究

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The hepatoprotective effect of dexamethasone was investigated in rats exposed to ischemia/ reperfusion liver injury. Ischemia was induced by clamping the pedicle of the left hepatic lobe for 1 h followed by 3 h of reperfusion. Dexamethasone was administered 24 h before the ischemic insult in two i.p., doses (10 mg kg~-1, each) with 12 h interval. Dexamethasone significantly attenuated the ischemia/reperfusion-induced elevations in serum aminotransferase and hepatic levels of tumor necrosis factor-alpha and nitric oxide. Dexamethasone also significantly compensated deficits in hepatic antioxidant defense mechanisms (reduced glutathione and catalase and superoxide dismutase activities) and suppressed lipid peroxidation observed with liver hypoxia-reoxygenation. This was associated with significant restoration of the ischemia/reperfusion-induced increase in hepatic caspase-3 activity. Neutrophilinfiltrationandhepatocellularnecrosis andapoptosis detected by histopathological examination of liver tissue were markedly ameliorated by pre-ischemic dexamethasone treatment.
机译:在暴露于缺血/再灌注肝损伤的大鼠中研究了地塞米松的肝脏保护作用。通过将左肝叶的椎弓根夹持1小时,诱导缺血,然后再灌注3小时。在缺血性侮辱前24小时施用地塞米松,两种I.P.,剂量(10mg kg〜-1,每个),12小时间隔。地塞洛塞显着减弱了血清氨基转移酶和肿瘤坏死因子-α和一氧化氮的肝脏水平的缺血/再灌注诱导的升高。地塞米松还显着补偿了肝脏抗氧化防御机制(降低谷胱甘肽和过氧化氢酶和超氧化物歧化酶活性)和用肝缺氧 - 雷氧化观察到的脂质过氧化。这与肝癌酶-3活性的缺血/再灌注诱导的升高的显着恢复有关。通过预缺血地塞米松治疗,通过肝组织组织病理学检查检测到检测到的中性粒细胞症和肺凋亡。

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