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首页> 外文期刊>Tropical Journal of Pharmaceutical Research >Sevoflurane improves gaseous exchange and exerts protective effects in lipopolysaccharide-induced lung injury in mice models
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Sevoflurane improves gaseous exchange and exerts protective effects in lipopolysaccharide-induced lung injury in mice models

机译:七氟醚改善气体交换并在脂多糖诱导的小鼠肺损伤模型中发挥保护作用

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Purpose: To investigate the protective effect of sevoflurane against lipopolysaccharide (LPS)-induced acute liver injury (ALI) in amice model. Methods: Seven week-old female BalB/C mice were used. Lung water content and cell count were estimated by standard protocols. Cytokine and chemokine analysis was performed using commercially available kits. Myeloperoxidase activity was evaluated spectrophotometrically while histopathological analysis was carried out by H and E staining. Results: The results revealed that sevoflurane treatment significantly improved gaseous exchange, and reduced lung water content and lung inflammation as evidenced by a decrease in neutrophil migration into BALF (p 0.01). Sevoflurane also significantly reversed the LPS-triggered suppression of IL-10 in the lung tissues of LPS-treated mice, when compared to saline-treated controls (p 0.01). It reversed LPS-induced oxidative stress, as demonstrated by increase in total antioxidant capacity (T-AC), catalase (CAT) and superoxide dismutase-1 (SOD-1), as well as an increase in reduced/oxidized glutathione (GSH/GSSG) ratio. In addition, sevoflurane blocked LPS-induced lung tissue injury in ALI mice, and exerted protective effects against acute LPS-induced lung injury. Conclusion: These results suggest that sevoflurane improves gaseous exchange and exerts a protective effect against LPS-triggered lung injury in mice model, most probably due to its anti-inflammatory and antioxidant properties.
机译:目的:探讨七氟醚对脂多糖(LPS)引起的急性肝损伤(ALI)的保护作用。方法:使用7周龄的雌性BalB / C小鼠。肺水含量和细胞计数通过标准方案估算。细胞因子和趋化因子分析是使用市售试剂盒进行的。分光光度法评价髓过氧化物酶活性,同时通过H和E染色进行组织病理学分析。结果:结果显示七氟醚治疗显着改善了气体交换,并减少了肺水含量和肺部炎症,这可通过嗜中性粒细胞向BALF迁移的减少来证明(p <0.01)。与盐水对照组相比,七氟醚还可以显着逆转LPS刺激的小鼠肺组织中LPS触发的IL-10抑制(p <0.01)。它逆转了LPS诱导的氧化应激,如总抗氧化能力(T-AC),过氧化氢酶(CAT)和超氧化物歧化酶-1(SOD-1)增加以及还原/氧化型谷胱甘肽(GSH / GSSG)比率。此外,七氟醚可阻断LPS诱导的ALI小鼠肺组织损伤,并对急性LPS诱导的肺损伤具有保护作用。结论:这些结果表明,七氟醚可改善小鼠模型中的气体交换并具有抵抗LPS触发的肺损伤的保护作用,这很可能是由于其抗炎和抗氧化特性。

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