title: Protective effects of valsartan against cigarette smoke-induced left ventricular systolic dysfunction in rats.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, People's Republic of China. zhou-xiang@suda.edu.cn
authors.forename: Xiang
authors.initials: X
authors.lastname: Zhou
authors.forename: Chao
authors.initials: C
authors.lastname: Li
authors.forename: Weiting
authors.initials: W
authors.lastname: Xu
authors.forename: Jianchang
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012907:Smoking / Q000009:adverse effects* / Q000188:drug therapy* / Q000503:physiopathology; D013777:Tetrazoles / Q000494:pharmacology / Q000627:therapeutic use*; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D000068756:Valsartan; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control*
chemical_list: D002316:Cardiotonic Agents; D018836:Inflammation Mediators; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine