PMID- 33766229 OWN - NLM STAT- MEDLINE DCOM- 20210329 LR - 20211204 IS - 1007-8738 (Print) IS - 1007-8738 (Linking) VI - 37 IP - 3 DP - 2021 Mar TI - [Astragaloside II inhibits the proliferation of rat pulmonary artery smooth muscle cells induced by hypoxia via blocking NOX/ROS/AKT/mTOR signaling pathway]. PG - 219-224 AB - Objective To investigate the inhibitory effect of astragaloside II (AS-II) on the proliferation of pulmonary artery smooth muscle cells (PASMCs) induced by hypoxia and its relevant mechanism. Methods Rat primary PASMCs were divided into normoxia group, hypoxia group, hypoxia combined with 20, 40, 80 mumol/L AS-II treated groups, hypoxia combined with nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) inhibitor VAS2870 treated group, and then cultured either in normoxic (210 mL/L O(2)) or hypoxic (20 mL/L O(2)) condition for 24 hours. The proliferation of PASMCs was detected by CCK-8 assay. The level of intracellular reactive oxygen species (ROS) was detected by DCFH-DA staining. Protein kinase B (AKT), phospho-AKT (p-AKT), mammalian target of rapamycin (mTOR), phospho-mTOR (p-mTOR), proliferating cell nuclear antigen (PCNA), NOX1 and NOX4 protein expression were assessed by Western blotting. Results In the hypoxia group, the proliferation of PASMCs, level of intracellular ROS, protein expression of PCNA, p-AKT, p-mTOR, NOX1 and NOX4 increased significantly compared with those in the normoxia group. However, AS-II treatment inhibited hypoxia-induced PASMCs proliferation, decreased the level of intracellular ROS, and suppressed protein expression of PCNA, p-AKT, p-mTOR, NOX1 and NOX4. Moreover, VAS2870 treatment lead to similar changes. Conclusion AS-II can inhibit the proliferation of PASMCs induced by hypoxia, which may be associated with the blocking of NOX/ROS/AKT/mTOR signaling pathway. FAU - Jin, Haifeng AU - Jin H AD - Department of Anatomy, Qigihar Institute of Medical and Pharmaceutical Sciences, Qiqihar Medical University, Qiqihar 161006, China. FAU - Yao, Lijie AU - Yao L AD - Department of Anatomy, Qiqihar Medical University, Qiqihar 161006, China. FAU - DU, Fengxia AU - DU F AD - Department of Etiology, Qiqihar Medical University, Qiqihar 161006, China. FAU - Jiang, Yang AU - Jiang Y AD - Department of Anatomy, Qiqihar Medical University, Qiqihar 161006, China. FAU - Li, Xuemei AU - Li X AD - Experiment and Practice Training Center, Qiqihar Medical University, Qiqihar 161006, China. FAU - Zhang, Yuting AU - Zhang Y AD - Department of Anatomy, Qiqihar Medical University, Qiqihar 161006, China. FAU - Wang, Guan AU - Wang G AD - Department of Anatomy, Qiqihar Medical University, Qiqihar 161006, China. FAU - Liu, Jicheng AU - Liu J AD - Qigihar Institute of Medical and Pharmaceutical Sciences, Qiqihar Medical University, Qiqihar 161006, China. *Corresponding authors, E-mail: jcliu@qmu.edu.cn. FAU - Zhou, Zhongguang AU - Zhou Z AD - Basic Discipline of Integrated Chinese and Western Medicine, Heilongjiang University of Chinese Medicine, Harbin 150000, China. *Corresponding authors, E-mail: zzg5709@163.com. LA - chi PT - Journal Article PL - China TA - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi JT - Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology JID - 101139110 RN - 0 (Reactive Oxygen Species) RN - 0 (Saponins) RN - 0 (astragaloside II) RN - EC 2.7.1.1 (mTOR protein, rat) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Animals MH - Cell Hypoxia MH - Cell Proliferation MH - Cells, Cultured MH - Hypoxia MH - Myocytes, Smooth Muscle/metabolism MH - *Proto-Oncogene Proteins c-akt/metabolism MH - *Pulmonary Artery/metabolism MH - Rats MH - Reactive Oxygen Species MH - Saponins MH - Signal Transduction MH - TOR Serine-Threonine Kinases EDAT- 2021/03/27 06:00 MHDA- 2021/03/30 06:00 CRDT- 2021/03/26 05:52 PHST- 2021/03/26 05:52 [entrez] PHST- 2021/03/27 06:00 [pubmed] PHST- 2021/03/30 06:00 [medline] PST - ppublish SO - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2021 Mar;37(3):219-224.