Exposure to carbon blacks (CBs) has been associated with the progression of pulmonary fibrosis, whereas the mechanism is still not clear. We therefore aimed to investigate the effect of RhoA/ROCK pathway on pulmonary fibrosis caused by CBs exposure. Western blot analysis indicated that CBs could promote the activation of RhoA/ROCK pathway and phosphorylation of p65 and IκBα in mice lung. However, ROCK inhibitor Y-27632 could attenuate phosphorylation levels of p65 and IκBα and restore histopathological changes of the lung tissue. Then, we evaluated the effect of RhoA/ROCK pathway on pulmonary fibrosis by detecting the expression levels of α-SMA, vimentin, and Collagen type-I (Col-I), which could be partly inhibited by Y-27632. It was assumed that inhibition of ROCK could be a promising therapeutic candidate for CBs-induced pulmonary fibrosis, which possibly through the blockage of RhoA/ROCK/NF-κB pathway.

中文翻译：

---

ROCK 抑制剂通过 Rho/ROCK/NF-kappa B 通路减弱炭黑诱导的小鼠肺纤维化

接触炭黑 (CBs) 与肺纤维化的进展有关，但其机制尚不清楚。因此，我们旨在研究 RhoA/ROCK 通路对 CBs 暴露引起的肺纤维化的影响。Western印迹分析表明CBs可以促进小鼠肺RhoA/ROCK通路的激活和p65和IκBα的磷酸化。然而，ROCK 抑制剂 Y-27632 可以减弱 p65 和 IκBα 的磷酸化水平并恢复肺组织的组织病理学变化。然后，我们通过检测 α-SMA、波形蛋白和 I 型胶原蛋白 (Col-I) 的表达水平来评估 RhoA/ROCK 通路对肺纤维化的影响，这些表达水平可以被 Y-27632 部分抑制。据推测，抑制 ROCK 可能是 CBs 诱导的肺纤维化的有希望的治疗候选者，