Abstract

Twenty five rabbits were randomized into five groups (n = 5): Normal Control group(NC) were kept on a plain chow diet for 75 days. AT group were kept on a hypercholesterolaemicdiet for 75 days. ATO (atorvastatin) group were fed the same diet and receivedatorvastatin orally (20mg/kg/day) from day 45 for 30 days. L group were fed thesame diet and intraperitoneal L-carnitine (250 mg/kg/day) from day 45 for 30 days (completionof treatment). ATO/L group were fed the same diet and atorvastatin orally(l0 mg/kg/day) and L-carnitine intraperitoneally (125 mg/kg/day) from day 45 for 30 days.Histopathological investigations of aorta and assessment of serum profile were carried out to determine Blood urea nitrogen (BUN), creatinine (Cr), Sodium (Na), potassium (K), Phosphorus (P), triglycerides (TG), total cholesterol, high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and Alkaline phosphatase(ALK). The aorta wall of hypercholesterolaemic rabbits showedfoam cells with disrupted endothelial lining and changed muscle fibers. The animals of ATO and ATO/L groups had normal aorta wall. TG significantly increased in hypercholesterolaemic rabbits.L-carnitine treatment significantly reduced TG (P 0.05) except for L group, where BUN level wassignificantly higherthan those in ATO and ATO/L groups (P<0.05). Serum AST, ALT and ALK levels were significantly reduced in L-carnitine treated animals compared to ATO group (P<0.05). L-carnitine prevented progression of atherosclerotic lesions.

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