Aloperine Suppresses Human Pulmonary Vascular Smooth Muscle Cell Proliferation Via Inhibiting Inflammatory Response
Aloperine Suppresses Human Pulmonary Vascular Smooth Muscle Cell Proliferation Via Inhibiting Inflammatory Response
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DOI：
10.4103/cjp.cjp_27_19
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发表时间：
2019-07-01
影响因子：
1.8
通讯作者：
Zhou, Ru
中科院分区：
文献类型：
--
作者：
Chang, Zhi;Zhang, Peng;Zhou, Ru
肺动脉血管平滑肌细胞（PASMCs）异常增殖是肺血管重塑的重要病理特征，是肺动脉高压（PAH）发生和发展的驱动力，最终导致肺动脉高压。苦豆碱是从传统中药苦豆子中提取的主要活性生物碱，具有突出的抗氧化、抗炎作用。本课题组前期研究发现Aloperine通过抑制氧化应激对monocroline诱导的大鼠肺动脉高压具有保护作用。然而，Aloperine 对 PAH 的抗炎作用仍不清楚。因此，为了进一步探讨 Aloperine 对 PAH 的有益作用是否与其抗炎作用有关，我们进行了体外实验。 Aloperine 显着抑制血小板源性生长因子-BB 诱导的人肺动脉平滑肌细胞 (HPASMC) 的增殖和 DNA 合成，阻断细胞周期 G(0)/G(1) 向 S 期的进展，并提高细胞凋亡的总比率。总之，这些结果表明 Aloperine 负向调节核因子-κ B 信号通路活性，对 PAH 产生保护作用，并抑制 HPASMC 增殖，因此在通过负向调节肺血管重塑来治疗肺动脉高压方面具有潜在价值。
Abnormal pulmonary arterial vascular smooth muscle cells (PASMCs) proliferation is critical pathological feature of pulmonary vascular remodeling that acts as driving force in the initiation and development of pulmonary arterial hypertension (PAH), ultimately leading to pulmonary hypertension. Aloperine is a main active alkaloid extracted from the traditional Chinese herbal Sophora alopecuroides and possesses outstanding antioxidation and anti-inflammatory effects. Our group found Aloperine has protective effects on monocroline-induced pulmonary hypertension in rats by inhibiting oxidative stress in previous researches. However, the anti-inflammation effects of Aloperine on PAH remain unclear. Therefore, to further explore whether the beneficial role of Aloperine on PAH was connected with its anti-inflammatory effects, we performed experiments in vitro. Aloperine significantly inhibited the proliferation and DNA synthesis of human pulmonary artery smooth muscle cells (HPASMCs) induced by platelet-derived growth factor-BB, blocked progression through G(0)/G(1) to S phase of the cell cycle and promoted total ratio of apoptosis. In summary, these results suggested that Aloperine negatively regulated nuclear factor-kappa B signaling pathway activity to exert protective effects on PAH and suppressed HPASMCs proliferation therefore has a potential value in the treatment of pulmonary hypertension by negatively modulating pulmonary vascular remodeling.