TY -的A2 Sipert卡拉盟,张歌AU -阴,ZongXiu盟——秦WeiDong AU - Ma,小丽张盟——姚明盟——刘翔,EnXiu盟——楚YanBiao PY - 2020 DA - 2020/06/11 TI - Pirfenidone抑制缺氧肺动脉高压通过NADPH / ROS p38通路外膜成纤维细胞在肺动脉SP - 2604967六世- 2020 AB -缺氧肺动脉高压(HPH)是一种破坏性疾病,其特征是进行性血管收缩和血管重建。Pirfenidone (PFD)抑制HPH的进展,尽管分子机制仍不明。本研究旨在确定PFD在HPH的作用和机制在人类肺动脉外膜成纤维细胞(HPAAFs),这是在正常或低氧条件下培养。NOX4和Rac1抑制或过表达的成分或pcDNA3.1,分别。扩散HPAAFs量化了比色3 - (4 5-dimethylthiazol-2-yl) 2, 5-diphenyltetrazolium (MTT)分析评估细胞代谢活动,细胞计数,ethynyldeoxyuridine (EdU)化验检测DNA合成。迁移HPAAFs被一个伤口愈合试验评估。表达水平的平滑肌alpha-actin (a-SMA)及胶原我(COL1A1)评估通过rt - pcr和免疫印迹分析。PFD HPAAFs抑制低氧诱导增殖和迁移。与低氧对照组相比,PFD减少a-SMA及胶原的表达我(COL1A1)。PFD减少低氧诱导的磷酸化p38通过NOX4 /活性氧(ROS)信号通路。 Moreover, Rac1 also decreased hypoxia-induced phosphorylation of p38, without any cross-interaction with NOX4. These findings demonstrate that PFD is a novel therapeutic agent to prevent cell proliferation, migration, and fibrosis, which might be useful in inhibiting vascular remodeling in patients with HPH. SN - 0962-9351 UR - https://doi.org/10.1155/2020/2604967 DO - 10.1155/2020/2604967 JF - Mediators of Inflammation PB - Hindawi KW - ER -