%0 Journal Article
%T Antihyperlipidemic and Antioxidant Potential of Paeonia emodi Royle against High-Fat Diet Induced Oxidative Stress
%A Bilal A. Zargar
%A Mubashir H. Masoodi
%A Bahar Ahmed
%A Showkat A. Ganie
%J ISRN Pharmacology
%D 2014
%R 10.1155/2014/182362
%X The present study was intended to evaluate the effects of Paeonia emodi rhizome extracts on serum triglycerides (TGs), total cholesterol (TC), low density lipoprotein cholesterol (LDL-c), high density lipoprotein cholesterol (HDL-c), atherogenic index (AI), superoxide dismutase (SOD), and glutathione peroxidase (GPx). The plant was extensively examined for its in vitro antioxidant activity, and the preliminary phytochemical screening was carried out using standard protocols. Male Wistar rats were induced with hyperlipidemia using high-fat diet and were treated orally with hydroalcoholic and aqueous extracts at the dose of 200£¿mg/kg bw for 30 days. TGs, TC, LDL-c, and AI were significantly reduced while HDL-c, SOD, and GPx levels rose to a considerable extent. After subjecting to acute toxicity testing, the extracts were found to be safe. The observations suggest antihyperlipidemic and antioxidant potential of P. emodi in high-fat diet induced hyperlipidemic/oxidative stressed rats. 1. Introduction Reactive oxygen species (ROS) comprises superoxide, hydroxyl, peroxyl ( ), alkoxyl ( ), and hydroperoxyl ( ) radicals. Nitric oxide and nitrogen dioxide ( ) are two nitrogen free radicals. Oxygen and nitrogen free radicals can be converted to other nonradical reactive species, such as hydrogen peroxide, hypochlorous acid (HOCl), and peroxynitrite ( ). ROS, reactive nitrogen species (RNS), and reactive chlorine species are generated in aerobic cells under physiologic and pathologic conditions [1]. Thus, ROS and RNS include radical and nonradical species. These species are maintained at very low steady-state concentration by the antioxidant system, but when their production increases they may overcome the scavenger capacity of the antioxidant system, resulting in an oxidative stress and damage to biological targets. Plasma lipoproteins are protected against oxidative modification by the antioxidant defense system of the organism. This system is constituted by the enzymes like SOD, glutathione peroxidase (GPx), and catalase, as well as hydrophilic antioxidants such as ascorbate, reduced glutathione, and urate. Lipoprotein particles carry lipophilic antioxidants, such as tocopherols and carotenoids. All of these interact with free radicals or block free radical chain reactions [2]. Endothelial cells, smooth muscle cells, and macrophages are the sources of oxidants for the oxidative modification of phospholipids. Ox-LDL can damage endothelial cells and induce the expression of adhesion molecules such as P-selectin and chemotactic factors such as monocyte
%U http://www.hindawi.com/journals/isrn.pharmacology/2014/182362/