Abstract
Hypoxia-induced pulmonary arterial hypertension (HPAH) is due to hypoxia caused by vascular endothelial cell remolding and damage. Previous studies have suggested that CX3CL1 plays an important role in HPAH which is affected by oxidative stress. Ca2+ channel activation correlated with increasing NF-κB levels induced by ROS. Tanreqing injection (TRQ) is a traditional Chinese medicine (TCM) for acute upper respiratory tract infection and acute pneumonia. In the present study, we explored the effect of TRQ on human pulmonary artery smooth muscle cells (HPASMCs) undergoing hypoxia and feasible molecular mechanisms involved in. Cell proliferation was assayed using CCK8 kits. Immunofluorescence and western blotting along with ELISA assay were performed to investigate the effect of TRQ on hypoxia-induced ROS, Ca2+, hydroxyl free radicals, and the expression of Ca2+ channel protein TRPC1, CX3CR1, HIF-1α, NF-κBp65, and p-NF-κBp65 in HPASMCs. Human CX3CL1 and the inhibitor of TRPC1 as SKF96365 were used for further investigation. TRQ inhibited hypoxia-induced increasing cell adhesion, ROS, Ca2+, hydroxyl free radicals, CX3CR1, HIF-1α, NF-κBp65 activation, and even on TRPC1 expression in HPASMC which tended to be attenuated even reversed by CX3CL1. Our results suggested that TRQ might help to attenuate remodeling of HPASMC through inhibiting the ROS and TRPC1/CX3CL1 signaling pathway.
Highlights
Hypoxia may induce increased pulmonary arterial pressure and pulmonary vascular resistance, which is involved in hypoxia-induced pulmonary arterial hypertension (HPAH) [1, 2]
We explored the effect of Tanreqing injection (TRQ) on human pulmonary Artery Smooth Muscle Cells (HPASMCs) undergoing hypoxia and feasible molecular mechanisms
Cell proliferation of human pulmonary artery smooth muscle cells (HPASMCs) is involved in pulmonary arterial hypertension, and we explored the effect of TRQ, CX3CX1, cysteine, and TRP channels (TRPC) inhibitor SKF96365 on cell proliferation of HPASMCs using MTT assay
Summary
Hypoxia may induce increased pulmonary arterial pressure and pulmonary vascular resistance, which is involved in hypoxia-induced pulmonary arterial hypertension (HPAH) [1, 2]. HPAH is due to hypoxia-induced vascular endothelial cell damage, pulmonary vasoconstriction (HPV), increased vascular tension, pulmonary vascular remodeling, etc., to result in continuous increasing pulmonary artery pressure and eventually lead to increasing right ventricular afterload, ventricular remodeling, and heart failure. The pathogenesis of HPAH is very complicated, and there have been many studies on its potential mechanism At present, it mainly includes the direct factors of hypoxia, humoral factors, ion channels (calcium channels/potassium channels), and gene changes, among which inflammatory reaction, Oxidative Medicine and Cellular Longevity oxidative stress [11, 12], membrane ion channel imbalance [13], and other factors may play a key role. The cells in the vasculature layers, as pulmonary artery smooth muscle cells (PASMCs) were concerned, are characterized by hyperproliferation to induced remodeling to lead to increased resistance of blood vessel and result in right heart failure and death eventually [15, 16].
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