Background

Nisoldipine can effectively suppress pulmonary arterial smooth muscle cell proliferation and c-Fos expression.

Objective

To identify the mechanism of the anti-inflammatory effects in monocrotaline-induced pulmonary arterial hypertension (PAH), focusing on the c-Fos/NLRP3/caspase-1 pathway.

Results

In a mice model of monocrotaline-induced PAH, miRNA-155 expression was increased. In an in vitro model, overexpression of miRNA-155 promoted inflammation and induced c-Fos, NLRP3, and caspase-1 protein expression. The inhibition of c-Fos reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH. The inhibition of NLRP3 reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH.

Conclusions

miRNA-155 increased inflammation in monocrotaline-induced PAH through c-Fos/NLRP3/caspase-1.

中文翻译：

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miRNA-155通过c-Fos / NLRP3 / caspase-1在一克他吗啉诱导的肺动脉高压中的作用

背景

尼索地平可以有效抑制肺动脉平滑肌细胞增殖和c-Fos表达。

目的

为了确定在单crocrotaline诱导的肺动脉高压（PAH）中抗炎作用的机制，重点是c-Fos / NLRP3 / caspase-1途径。

结果

在单crocrotaline诱导的PAH的小鼠模型中，miRNA-155表达增加。在体外模型中，miRNA-155的过表达促进炎症并诱导c-Fos，NLRP3和caspase-1蛋白表达。c-Fos的抑制作用在苦味碱诱导的PAH体外模型中降低了miRNA-155对炎症的影响。NLRP3的抑制作用在苦味碱诱导的PAH体外模型中降低了miRNA-155对炎症的影响。

结论

miRNA-155通过c-Fos / NLRP3 / caspase-1增强了苦瓜碱诱导的PAH中的炎症。