School of Life Science, Shaoxing University, Shaoxing, China.
College of Life and Environmental Science, Hangzhou Normal University, Hangzhou, China.
Environ Toxicol. 2021 Jul;36(7):1476-1484. doi: 10.1002/tox.23135. Epub 2021 Mar 31.
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.
暴露于炭黑 (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 blot 分析表明，CBs 可促进小鼠肺中 RhoA/ROCK 通路的激活以及 p65 和 IκBα 的磷酸化。然而，ROCK 抑制剂 Y-27632 可降低 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 (Col-I) 的表达水平来评估 RhoA/ROCK 通路对肺纤维化的影响，Y-27632 可部分抑制这些表达水平。据推测，抑制 ROCK 可能是 CBs 诱导的肺纤维化的一种有前途的治疗候选物，其可能通过阻断 RhoA/ROCK/NF-κB 通路。
