博莱霉素
医学
地塞米松
肺纤维化
STAT1
纤维化
斯达
肺
转化生长因子
癌症研究
炎症
JAK-STAT信号通路
肺纤维化
免疫学
作者
Keyun Shi,Jianzhong Jiang,Tieliang Ma,Jing Xie,Lirong Duan,Ruhua Chen,Ping Song,Zhixin Yu,Chao Liu,Qin Zhu,Jinxu Zheng
摘要
In order to find the possible mechanism of Dexamethasone (Dex) during curing fibrosis, the bleomycin (BLM)-induced mice model was used. After fibrosis were induced by BLM, histopathological evaluation and RT-PCR were employed to detect the expression of TGF-β1, Smad3 and STAT1. It was found that BLM promoted the development of inflammation, leading to severe pulmonary fibrosis with the increasing of TGF-β1, Smad3 and STAT1. After Dex treatment, the expression of TGF-β1, Smad3 and STAT1 showed a little higher with alleviation of the fibrosis. Thus it is concluded that there is a possible pathway of mouse pulmonary fibrosis model through TGF-β, Smad3 and JAK-STAT pathway.
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