TY - JOUR ID - 20386 TI - Cigarette smoke extract stimulates human pulmonary artery smooth muscle cell proliferation: Role of inflammation and oxidative stress JO - Iranian Journal of Basic Medical Sciences JA - IJBMS LA - en SN - 2008-3866 AU - Wang, Juan AU - Wang, Le AU - Chen, Xing AU - Liang, Mao-Li AU - Wei, Dong-Hui AU - Cao, Jie AU - Zhang, Jing AD - Department of Respiratory and Critical Care Medicine, Tianjin Medical University General Hospital, Tianjin 300052, China Y1 - 2022 PY - 2022 VL - 25 IS - 6 SP - 755 EP - 761 KW - Cigarette Smoking KW - Pulmonary arterial - hypertension KW - Inflammation KW - NF-κB KW - Oxidative stress DO - 10.22038/ijbms.2022.64170.14133 N2 - Objective(s): Cigarette smoke may play a direct role in proliferation of human pulmonary artery smooth muscle cells (HPASMCs). However, the mechanism involved and the effect of interventions remain unclear. We aimed to evaluate the effect of cigarette smoke extract (CSE) on HPASMCs, explore the role of inflammation and oxidative stress, and the effects of Tempol and PDTC in this process.Materials and Methods: HPASMCs were subjected to normal control (NC), CSE, CSE+Tempol (CSE+T), and CSE+PDTC (CSE+P) groups. Proliferation of HPASMCs was measured by CCK-8 and Western blot. TNF-α, IL-6, MDA, and SOD levels were determined by ELISA and commercial kits. Nuclear translocation of NF-κB p65 was evaluated by western blot.Results: 1%, 2.5%, and 5% CSE all promoted proliferation of HPASMCs, and effect of 1% CSE was the most significant, however, 7.5% and 10% CSE inhibited viability of cells (all P<0.05). Compared with the NC group, TNF-α, IL-6, and MDA levels increased, SOD activity decreased (all P<0.05), and NF-κB p65 expression in nuclei increased (P=0.04) in the CSE group. Tempol and PDTC inhibited the proliferation of HPASMCs induced by CSE (all P<0.05). And compared with the CSE group, TNF-α, IL-6, and MDA levels in CSE+T and CSE+P groups decreased, while SOD activity increased (all P<0.05). Tempol reduced the expression of NF-κB p65 in nuclei but did not achieve a significant difference (P=0.08). PDTC inhibited the nuclear translocation of NF-κB p65 (P=0.03).Conclusion: CSE stimulates HPASMCs proliferation in a certain concentration range. The CSE-induced proliferation of HPASMCs involved excessive inflammatory response and oxidative stress. Tempol and PDTC attenuate these effects of CSE on HPASMCs. UR - https://ijbms.mums.ac.ir/article_20386.html L1 - https://ijbms.mums.ac.ir/article_20386_cab6b2e6b0f6eaec1bb5465f30e10cf1.pdf ER -