Xiang Zhou1, Chao Li, Weiting Xu, Jianchang Chen. 1. Department of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, People's Republic of China. zhou-xiang@suda.edu.cn
Abstract
OBJECTIVES: To investigate the protective effects of valsartan against smoking-induced left ventricular dysfunction and explore the potential mechanisms involved. METHODS: Rats were randomly divided into 3 groups: smoking group (exposed to cigarette smoke), valsartan group (exposed to cigarette smoke and treated orally with valsartan), and control group. Transthoracic echocardiography was performed to evaluate left ventricular systolic and diastolic function. Oxidative stress was evaluated by detecting malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the supernatant of left ventricular tissue. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-a (TNF-α), and monocyte chemotactic protein-1 (MCP-1) were detected to reflect the extent of systemic inflammation. RESULTS: The echocardiographic data indicated that valsartan has protective effects against cigarette smoke-induced left ventricular systolic dysfunction (LVSD). Our findings showed a significant decrease in MDA level and increases in SOD and GSH-Px activities in the valsartan group compared to the smoking group. The apoptotic rate in the valsartan group was significantly lower than in the smoking group. The concentrations of hs-CRP, IL-6, TNF-α and MCP-1 in the valsartan group were significantly lower than in the smoking group. CONCLUSIONS: Our study demonstrates that valsartan has protective effects against smoking-induced LVSD by attenuating oxidative stress, apoptosis, and inflammation.
OBJECTIVES: To investigate the protective effects of valsartan against smoking-induced left ventricular dysfunction and explore the potential mechanisms involved. METHODS:Rats were randomly divided into 3 groups: smoking group (exposed to cigarette smoke), valsartan group (exposed to cigarette smoke and treated orally with valsartan), and control group. Transthoracic echocardiography was performed to evaluate left ventricular systolic and diastolic function. Oxidative stress was evaluated by detecting malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the supernatant of left ventricular tissue. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumornecrosis factor-a (TNF-α), and monocyte chemotactic protein-1 (MCP-1) were detected to reflect the extent of systemic inflammation. RESULTS: The echocardiographic data indicated that valsartan has protective effects against cigarette smoke-induced left ventricular systolic dysfunction (LVSD). Our findings showed a significant decrease in MDA level and increases in SOD and GSH-Px activities in the valsartan group compared to the smoking group. The apoptotic rate in the valsartan group was significantly lower than in the smoking group. The concentrations of hs-CRP, IL-6, TNF-α and MCP-1 in the valsartan group were significantly lower than in the smoking group. CONCLUSIONS: Our study demonstrates that valsartan has protective effects against smoking-induced LVSD by attenuating oxidative stress, apoptosis, and inflammation.
Authors: Abdullah Kaplan; Emna Abidi; Rana Ghali; George W Booz; Firas Kobeissy; Fouad A Zouein Journal: Oxid Med Cell Longev Date: 2017-07-20 Impact factor: 6.543