%0 Journal Article
%T Antihyperlipidemic Activity of Aloe succotrina in Rats: Possibly Mediated by Inhibition of HMG-CoA Reductase
%A Dinesh Dhingra
%A Deepak Lamba
%A Ramesh Kumar
%A Pashupati Nath
%A Satyaprakash Gauttam
%J ISRN Pharmacology
%D 2014
%R 10.1155/2014/243575
%X The present study was designed to investigate antihyperlipidemic activity of dried pulp of Aloe succotrina leaves in Wistar albino rats. Hyperlipidemia was induced in rats by feeding them high fat diet (HFD) or D-fructose (25%£¿w/v) for 4 successive weeks. From 15th to 28th day, dried pulp (100 and 200£¿mg/kg, p.o) and atorvastatin (10£¿mg/kg, p.o.) per se were administered 2£¿h prior to feeding rats with HFD or fructose. Aloe succotrina did not significantly decrease the body weight of rats. The dried pulp and atorvastatin per se significantly decreased relative liver weight but did not significantly affect relative heart weight. HFD or fructose significantly increased serum total cholesterol, triglycerides, LDL-c, and VLDL, and decreased HDL-c; significantly increased liver MDA and decreased GSH levels. The dried pulp (200£¿mg/kg p.o.) significantly reversed high fat diet-induced and fructose-induced hyperlipidemia and atherogenic index. Aloe succotrina significantly decreased HMG Co-A reductase activity. Antihyperlipidemic effect of the dried pulp was comparable to atorvastatin. Thus, Aloe succotrina produced significant antihyperlipidemic activity in both HFD and fructose-induced hyperlipidemic rats, possibly through normalization of serum lipid profile, HMG-CoA reductase inhibitory activity, and amelioration of oxidative stress in liver. 1. Introduction Hyperlipidemia is a heterogeneous disorder commonly characterized by elevated serum total cholesterol, low density and very low-density lipoprotein cholesterol, triglycerides, and decreased high-density lipoprotein levels [1]. Hyperlipidemia is one of the greatest risk factors contributing to the prevalence and severity of atherosclerosis and subsequent coronary heart disease [2]. Liver synthesizes two-third of the total cholesterol made in the body. The rate limiting enzyme is 3-hydroxy-3-methylglutaryl (HMG)-Co A reductase and provides feedback regulation by controlling the cholesterol concentrations in cells. Treatment of hyperlipidemia involves diet control, exercise, and the use of lipid-lowering diets and drugs [3]. The most commonly employed drugs for treatment of hyperlipidemia include hydroxymethylglutarate coenzyme A (HMG-CoA) reductase inhibitors, also called as statins. Other drugs employed for treatment of hyperlipidemia include bile acid sequestrants (anion-exchange resins) such as cholestyramine and colestipol; fibrates such as clofibrate, gemfibrozil, fenofibrate, ciprofibrate, and bezafibrate; niacin; cholesterol absorption inhibitors such as ezetimibe; and omega-3-fatty acids [4]. In
%U http://www.hindawi.com/journals/isrn.pharmacology/2014/243575/