Modulation of impact of high fat diet in pathological and physiological left ventricular cardiac hypertrophy by fluvastatin.
The male Wistar rats were kept at high fat diet for 90 days and subjected to partial abdominal aortic constriction (PAAC) at 62nd and continued up to 90th day. Similarly, rats were kept at high fat diet for 90 days and subjected to chronic swimming training (CST) at 46th day and continued up to 90th day. Obesity was assessed by % age change in body weight, WHR ratio and adiposity index whereas cardiac hypertrophy was assessed by using index of cardiac hypertrophy, i.e., left ventricular weight, left ventricular weight to body weight, (LVW/BW), left ventricular wall thickness (LVWT), cardiomyocyte diameter, LV, protein content and collagen content. Further, mean arterial blood pressure (MABP) was also recorded. Oxidative stress was assessed by measuring the levels of thiobarbituric acid reactive species (TBARS), levels of superoxide anion generation and levels of reduced glutathione in left ventricular tissue. The PAAC and CST increased the index of cardiac hypertrophy. Moreover, PAAC has significantly increased MABP. Fluvastatin, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, significantly attenuated PAAC induced left ventricular cardiac hypertrophy and MABP whereas no significant change was observed in CST-induced cardiac hypertrophy. Furthermore, fluvastatin significantly attenuated the oxidative stress by decreasing the levels of TBARS and superoxide anion generation and increasing the levels of reduced glutathione. These results suggest that fluvastatin prevented the PAAC-induced cardiac hypertrophy.
Singh
Randhir
R
Cardiovascular Pharmacology Division, Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India. dahiya_rsd@rediffmail.com
Krishan
Pawan
P
D000818:Animals; D001012:Aorta, Abdominal; D001786:Blood Glucose / Q000032:analysis; D003094:Collagen / Q000032:analysis; D003250:Constriction; D004041:Dietary Fats / Q000633:toxicity*; D019422:Dietary Sucrose / Q000633:toxicity; D004353:Drug Evaluation, Preclinical; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use*; D000077340:Fluvastatin; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000150:complications / Q000188:drug therapy*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D007211:Indoles / Q000627:therapeutic use*; D015227:Lipid Peroxidation / Q000187:drug effects; D008055:Lipids / Q000097:blood; D008297:Male; D009124:Muscle Proteins / Q000032:analysis; D009765:Obesity / Q000150:complications / Q000209:etiology; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013481:Superoxides / Q000378:metabolism; D013550:Swimming; D020257:Ventricular Remodeling
D001786:Blood Glucose; D004041:Dietary Fats; D019422:Dietary Sucrose; D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D008055:Lipids; D009124:Muscle Proteins; D013481:Superoxides; D000077340:Fluvastatin; D003094:Collagen; D005978:Glutathione