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首页> 外文期刊>Experimental Animals >Oxymatrine attenuates lipopolysaccharide-induced acute lung injury by activating the epithelial sodium channel and suppressing the JNK signaling pathway
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Oxymatrine attenuates lipopolysaccharide-induced acute lung injury by activating the epithelial sodium channel and suppressing the JNK signaling pathway

机译：氧化苦参碱通过激活上皮钠通道和抑制JNK信号通路来减轻脂多糖诱导的急性肺损伤

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The epithelial sodium channel (ENaC) and mitogen-activated protein kinase (MAPK) pathway have been reported to be associated with the progression of acute lung injury (ALI). Oxymatrine (OMT) alone or combined with other drugs can ameliorate paraquat- or oleic acid-induced lung injury. However, the effect of OMT on lipopolysaccharide (LPS)-induced ALI remains unknown. The aim of the present study was to evaluate whether OMT can attenuate LPS-induced ALI through regulation of the ENaC and MAPK pathway using an ALI mouse model. Histological assessment of the lung and inflammatory cell counts in bronchoalveolar lavage fluid (BALF) were performed by H&E and Wright-Giemsa staining. The lung wet/dry (W/D) weight ratio and the levels of tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), ENaC subunits, and the MAPK pathway members were determined. Isolated type II rat alveolar epithelial cells were incubated with OMT 30 min before LPS stimulation to investigate the activation of ENaC and the MAPK pathway. The results showed that OMT remarkably alleviated histopathologic changes in lung and pulmonary edema, reduced inflammatory cell counts in BALF, and decreased TNF-α and CRP levels in a dose-dependent manner. OMT significantly increased the three subunits of ENaC proteins in vivo and in vitro , while it decreased p-ERK/ERK, p-p38/p38, and p-JNK/JNK ratios in vivo . However, only the JNK pathway was markedly inhibited in vitro following pretreatment with OMT. Collectively, the results suggested that OMT might alleviate LPS-induced ALI by elevating ENaC proteins and inhibiting the JNK signaling pathway.
机译：据报道，上皮钠通道（ENaC）和有丝分裂原激活的蛋白激酶（MAPK）途径与急性肺损伤（ALI）的进展有关。单独或与其他药物合用氧化苦参碱（OMT）可以减轻百草枯或油酸引起的肺损伤。但是，OMT对脂多糖（LPS）诱导的ALI的影响仍然未知。本研究的目的是评估OMT是否可以通过使用ALI小鼠模型调节ENaC和MAPK途径来减弱LPS诱导的ALI。通过H＆E和Wright-Giemsa染色对支气管肺泡灌洗液（BALF）中的肺和炎症细胞计数进行组织学评估。确定肺干/湿（W / D）重量比和肿瘤坏死因子-α（TNF-α），C反应蛋白（CRP），ENaC亚基和MAPK通路成员的水平。在LPS刺激之前，将分离的II型大鼠肺泡上皮细胞与OMT孵育30分钟，以研究ENaC的激活和MAPK途径。结果表明，OMT以剂量依赖性方式显着减轻了肺和肺水肿的组织病理学变化，减少了BALF中的炎症细胞数量，并降低了TNF-α和CRP水平。 OMT在体内和体外显着增加ENaC蛋白的三个亚基，而在体内则降低p-ERK / ERK，p-p38 / p38和p-JNK / JNK比率。但是，在用OMT预处理后，只有JNK途径在体外受到显着抑制。总的来说，该结果表明OMT可以通过升高ENaC蛋白和抑制JNK信号通路来减轻LPS诱导的ALI。

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