罗亚
Rho相关蛋白激酶
Rho激酶抑制剂
磷酸化
化学
肺纤维化
纤维化
免疫印迹
医学
癌症研究
药理学
信号转导
病理
生物化学
基因
作者
Junyan Yan,Yaxin Tang,Xin Zhong,Huarong Huang,Haonan Wei,Yulei Jin,Yanjiang He,Jinqiao Cao,Lei Jin,Baowei Hu
摘要
Abstract 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.
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