Open AccessAloperine suppresses human pulmonary vascular smooth muscle cell proliferation via inhibiting inflammatory response
Author(s) -
Zhi Chang,
Peng Zhang,
Min Zhang,
Jun Feng,
Zhiqiang Hu,
Jiamei Yang,
Yuhua Wu,
Ran Zhou
Publication year - 2019
Publication title -
chinese journal of physiology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.396
H-Index - 31
eISSN - 2666-0059
pISSN - 0304-4920
DOI - 10.4103/cjp.cjp_27_19
Subject(s) - pulmonary hypertension , vascular smooth muscle , apoptosis , inflammation , pharmacology , medicine , oxidative stress , pulmonary artery , lung , cancer research , immunology , smooth muscle , chemistry , biochemistry
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-κB 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.