Shi Keyun, Jiang Jianzhong, Ma Tieliang, Xie Jing, Duan Lirong, Chen Ruhua, Song Ping, Yu Zhixin, Liu Chao, Zhu Qin, Zheng Jinxu
Department of Geriatrics, The Affiliated Yixing Hospital of Jiangsu University Yixing, Jiangsu, China.
Central Laboratory, The Affiliated Yixing Hospital of Jiangsu University Yixing, Jiangsu, China.
Int J Clin Exp Med. 2014 Sep 15;7(9):2645-50. eCollection 2014.
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.
为了探究地塞米松（Dex）在治疗纤维化过程中的可能机制，采用了博来霉素（BLM）诱导的小鼠模型。在BLM诱导纤维化后，采用组织病理学评估和逆转录-聚合酶链反应（RT-PCR）检测转化生长因子-β1（TGF-β1）、Smad3和信号转导子与转录激活子1（STAT1）的表达。结果发现，BLM促进炎症发展，导致严重的肺纤维化，同时TGF-β1、Smad3和STAT1表达增加。Dex治疗后，TGF-β1、Smad3和STAT1的表达略有升高，纤维化有所减轻。因此得出结论，小鼠肺纤维化模型可能存在通过TGF-β、Smad3和JAK-STAT途径的通路。
