Yan Guosen, Wang Jinxia, Yi Tao, Cheng Junfen, Guo Haixu, He Yuan, Shui Xiaorong, Wu Zeyong, Huang Shian, Lei Wei
Laboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang, China.
Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Pulm Circ. 2019 Nov 5;9(4):2045894019878599. doi: 10.1177/2045894019878599. eCollection 2019 Oct-Dec.
Pulmonary arterial hypertension is a rapidly progressive and often fatal disease. As the pathogenesis of pulmonary arterial hypertension remains unclear, there is currently no good drug for pulmonary arterial hypertension and new therapy is desperately needed. This study investigated the effects and mechanism of baicalin on vascular remodeling in rats with pulmonary arterial hypertension. A rat pulmonary arterial hypertension model was constructed using intraperitoneal injection of monocrotaline, and different doses of baicalin were used to treat these rats. The mean pulmonary arterial pressure (mPAP) and right ventricular systolic pressure (RVSP) were measured with a right heart catheter. Moreover, the hearts were dissected to determine the right ventricular hypertrophy index (RVHI). The lung tissues were stained with H&E and Masson's staining to estimate the pulmonary vascular remodeling and collagen fibrosis, and the expression of proteins in the AKT, ERK, and NF-κB p65 phosphorylation (p-AKT, p-ERK, p-p65) was examined by Western blot analysis. We found that compared with untreated pulmonary arterial hypertension rats, baicalin ameliorated pulmonary vascular remodeling and cardiorespiratory injury, inhibited p-p65 and p-ERK expression, and promoted p-AKT and p-eNOS expression. In conclusion, baicalin interfered with pulmonary vascular remodeling and pulmonary arterial hypertension development in rats through the AKT/eNOS, ERK and NF-κB signaling pathways.
肺动脉高压是一种进展迅速且往往致命的疾病。由于肺动脉高压的发病机制尚不清楚，目前尚无治疗肺动脉高压的有效药物，因此迫切需要新的治疗方法。本研究探讨了黄芩苷对肺动脉高压大鼠血管重塑的影响及其机制。采用腹腔注射野百合碱构建大鼠肺动脉高压模型，并用不同剂量的黄芩苷对大鼠进行治疗。采用右心导管测量平均肺动脉压（mPAP）和右心室收缩压（RVSP）。此外，解剖心脏以测定右心室肥厚指数（RVHI）。对肺组织进行苏木精-伊红（H&E）染色和Masson染色，以评估肺血管重塑和胶原纤维化情况，并通过蛋白质印迹分析检测AKT、ERK和NF-κB p65磷酸化（p-AKT、p-ERK、p-p65）蛋白的表达。我们发现，与未治疗的肺动脉高压大鼠相比，黄芩苷改善了肺血管重塑和心肺损伤，抑制了p-p65和p-ERK的表达，并促进了p-AKT和p-eNOS的表达。综上所述，黄芩苷通过AKT/eNOS、ERK和NF-κB信号通路干预大鼠肺血管重塑和肺动脉高压的发展。
