Affiliated Minzu Hospital of Guangxi Medical University, Department of Pulmonary and Critical Care Medicine, Nanning 530001, China.
Oxid Med Cell Longev. 2022 Feb 11;2022:3235102. doi: 10.1155/2022/3235102. eCollection 2022.
Hypoxia-induced pulmonary arterial hypertension (HPAH) is due to hypoxia caused by vascular endothelial cell remolding and damage. Previous studies have suggested that CX3CL1 plays an important role in HPAH which is affected by oxidative stress. Ca channel activation correlated with increasing NF-B levels induced by ROS. Tanreqing injection (TRQ) is a traditional Chinese medicine (TCM) for acute upper respiratory tract infection and acute pneumonia. In the present study, we explored the effect of TRQ on human pulmonary artery smooth muscle cells (HPASMCs) undergoing hypoxia and feasible molecular mechanisms involved in. Cell proliferation was assayed using CCK8 kits. Immunofluorescence and western blotting along with ELISA assay were performed to investigate the effect of TRQ on hypoxia-induced ROS, Ca, hydroxyl free radicals, and the expression of Ca channel protein TRPC1, CX3CR1, HIF-1, NF-Bp65, and p-NF-Bp65 in HPASMCs. Human CX3CL1 and the inhibitor of TRPC1 as SKF96365 were used for further investigation. TRQ inhibited hypoxia-induced increasing cell adhesion, ROS, Ca, hydroxyl free radicals, CX3CR1, HIF-1, NF-Bp65 activation, and even on TRPC1 expression in HPASMC which tended to be attenuated even reversed by CX3CL1. Our results suggested that TRQ might help to attenuate remodeling of HPASMC through inhibiting the ROS and TRPC1/CX3CL1 signaling pathway.
缺氧诱导性肺动脉高压（HPAH）是由于血管内皮细胞重塑和损伤引起的缺氧所致。先前的研究表明，CX3CL1 在 HPAH 中起重要作用，其受氧化应激影响。Ca 通道的激活与 ROS 诱导的 NF-B 水平的增加相关。痰热清注射液（TRQ）是一种用于治疗急性上呼吸道感染和急性肺炎的中药。在本研究中，我们探讨了 TRQ 对缺氧人肺动脉平滑肌细胞（HPASMC）的作用及其可能的分子机制。通过 CCK8 试剂盒测定细胞增殖。通过免疫荧光和 Western blot 以及 ELISA 测定来研究 TRQ 对缺氧诱导的 ROS、Ca、羟自由基以及 Ca 通道蛋白 TRPC1、CX3CR1、HIF-1、NF-Bp65 和 p-NF-Bp65 在 HPASMC 中的表达的影响。使用人 CX3CL1 和 TRPC1 的抑制剂 SKF96365 进行进一步研究。TRQ 抑制了缺氧诱导的细胞黏附、ROS、Ca、羟自由基、CX3CR1、HIF-1、NF-Bp65 激活的增加，甚至对 HPASMC 中 TRPC1 的表达也有抑制作用，而 CX3CL1 则有减弱甚至逆转的趋势。我们的研究结果表明，TRQ 可能通过抑制 ROS 和 TRPC1/CX3CL1 信号通路来帮助减轻 HPASMC 的重塑。
