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摘要
Objective This study aims to determine the effects of astragaloside Ⅳ (AS-Ⅳ) treatment on the viability, proliferation and migration of hypoxia-stimulated human pulmonary arterial smooth muscle cells (PASMCs), and to explore the underlying molecular mechanisms. Methods The mRNA and protein expression levels of proliferating cell nuclear antigen (PCNA) were determined qRT-PCR and Western blot assays, respectively. Cell viability and cell proliferation were determined by CCK-8 and 5-ethynyl-2′-deoxyuridine (EdU) cell proliferation assays, respectively. The cell migration was determined by Transwell migration assay. Results Hypoxia stimulation up-regulated the mRNA and protein expression of PCNA in PASMCs (P<0.05); hypoxia stimulation significantly promoted PASMC viability and proliferation (P<0.05), and also increased the migration of PASMCs (P<0.05). AS - Ⅳ concentration-dependently down-regulated the mRNA expression and protein expression of PCNA (P<0.05), inhibited the viability, proliferation and migration of PASMCs under hypoxia (P<0.05). Hypoxia stimulation activated the Wnt/β-catenin signaling in PASMCs; while AS-Ⅳ concentration-dependently repressed the Wnt/βcatenin signaling in the hypoxia-stimulated PASMCs (P<0.05). Moreover, the treatment of XAV393, a Wnt/β - catenin inhibitor, attenuated the hypoxia-induced increase in the viability, proliferation and migration of PASMCs (P<0.05). The treatment of LiCl, a Wnt/β - catenin activator, restored the mRNA and protein expression levels of PCNA in the hypoxia-stimulated PASMCs with AS-Ⅳ treatment (P<0.05). The inhibitory effects of AS-Ⅳ treatment on the viability, proliferation and migration of PASMCs under hypoxia was attenuated by LiCl treatment (P<0.05). Conclusion Our results indicate that AS-Ⅳ reversed hypoxia-induced proliferation and migration of human pulmonary artery smooth muscle cells, which may be by regulating the Wnt/β-catenin signaling pathway. ? 2022 China Tropical Medicine.
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