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氧化槐果碱抑制呼吸道合胞病毒诱导的肺损伤。

Oxysophocarpine inhibits lung injury induced by respiratory syncytial virus.

作者信息

Gao Jie, Li Ying, Wang Qiwei, Ma Xiaojian, Zhang Yan

机构信息

Department of Pediatrics, Henan University Huaihe HospitalKaifeng 475000, Henan, P. R. China.

出版信息

Am J Transl Res. 2017 Sep 15;9(9):4083-4093. eCollection 2017.

Abstract

Oxysophocarpine (OSC) has various pharmacological effects. This study was designed to investigate whether OSC confers protection against respiratory syncytial virus (RSV) infection-induced lung injury. Here, we found that OSC inhibited RSV replication and increased the viability of RSV-infected lung epithelial A549 cells. OSC suppressed the RSV-increased production and release of pro-inflammatory cytokines and chemokines [tumor necrosis factor-α, interleukin-6 (IL-6), IL-8, regulated on activation in normal T-cell expressed and secreted, macrophage inflammatory protein-1α; and monocyte chemoattractant protein-1] in A549 cells. OSC also reduced the formation of reactive oxygen species and enhanced the activities of antioxidant enzymes in RSV-infected cells. The anti-oxidative effect of OSC on RSV-infected cells was dependent on NF-E2-related factor 2 activation. In vivo, OSC significantly alleviated RSV-triggered mouse lung injury. Overall, these results indicated that OSC attenuates RSV-enhanced pulmonary damage by inhibiting oxidative stress and inflammation.

摘要

氧化槐果碱(OSC)具有多种药理作用。本研究旨在探讨OSC是否能对呼吸道合胞病毒(RSV)感染诱导的肺损伤起到保护作用。在此,我们发现OSC可抑制RSV复制,并提高受RSV感染的肺上皮A549细胞的活力。OSC抑制了A549细胞中RSV诱导增加的促炎细胞因子和趋化因子[肿瘤坏死因子-α、白细胞介素-6(IL-6)、IL-8、正常T细胞表达和分泌的激活调节因子、巨噬细胞炎性蛋白-1α;以及单核细胞趋化蛋白-1]的产生和释放。OSC还减少了活性氧的形成,并增强了受RSV感染细胞中抗氧化酶的活性。OSC对受RSV感染细胞抗氧化作用依赖于核因子E2相关因子2的激活。在体内,OSC显著减轻了RSV引发的小鼠肺损伤。总体而言,这些结果表明OSC通过抑制氧化应激和炎症来减轻RSV加重的肺部损伤。

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