Gong Jing, Li Huihua, Cui Xiaoqing, Yan Yuling, Yu Qinghe, Ding Qi, Shi Yuanyuan, Wang Peng
Traditional Chinese Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, Guangdong Province, China.
Shenzhen Research Institute, Beijing University of Chinese Medicine, Shenzhen, 518118, Guangdong Province, China.
J Ethnopharmacol. 2025 Mar 13;343:119395. doi: 10.1016/j.jep.2025.119395. Epub 2025 Feb 3.
Pulmonary hypertension (PH) is a serious and progressive disease, posing a significant challenge to patient survival and quality of life. However, current treatments have limited effectiveness. Tianlong Kechuanling (TL) is a traditional Chinese medicine (TCM) compound formulation commonly used in clinical practice for the treatment of pulmonary heart disease, but its underlying mechanism is unknown.
This study aimed to validate the mitigating effect of TL on PH and to further investigate its mechanism.
A rat model of PH was induced by SU5416 combined with hypoxia (SuHx). The effects of TL on PH were evaluated through right ventricular systolic pressure (RVSP), Right ventricular hypertrophy index (RVHI) and histopathological analysis. The serum levels of HIF-1α, VEGFA in rats were detected by ELISA; VEGFR2, Vimentin and CD31 were detected by immunohistochemistry to explore the mechanism of action of TL. Human pulmonary artery endothelial cells (HPAECs) were induced by hypoxia, and the effects of TL were confirmed by RT-PCR and Western Blotting. Liquid chromatography-mass spectrometry (LC-MS) analysis was used to identify the chemical composition of TL.
TL ameliorated PH through modulation of the HIF-1α/VEGFA pathway and endothelial-to-mesenchymal transition (End-MT). The study also identified the key chemical components responsible for these effects.
The study demonstrates that TL can improve PH by inhibiting End-MT, supporting the further development of TL as an effective therapeutic option for PH.
肺动脉高压（PH）是一种严重的进行性疾病，对患者的生存和生活质量构成重大挑战。然而，目前的治疗效果有限。天龙咳喘灵（TL）是一种在临床实践中常用于治疗肺心病的中药复方制剂，但其潜在机制尚不清楚。
本研究旨在验证TL对PH的缓解作用，并进一步探讨其机制。
采用SU5416联合低氧（SuHx）诱导大鼠PH模型。通过右心室收缩压（RVSP）、右心室肥厚指数（RVHI）和组织病理学分析评估TL对PH的影响。采用ELISA法检测大鼠血清中HIF-1α、VEGFA水平；采用免疫组织化学法检测VEGFR2、波形蛋白和CD31，以探讨TL的作用机制。对人肺动脉内皮细胞（HPAECs）进行低氧诱导，通过RT-PCR和Western Blotting法验证TL的作用。采用液相色谱-质谱（LC-MS）分析法鉴定TL的化学成分。
TL通过调节HIF-1α/VEGFA通路和内皮-间充质转化（End-MT）改善PH。该研究还确定了产生这些作用的关键化学成分。
该研究表明，TL可通过抑制End-MT改善PH，支持将TL进一步开发为治疗PH的有效治疗选择。
