Hypolipidaemic effects and mechanisms of the main component of Opuntia dillenii Haw. polysaccharides in high-fat emulsion-induced hyperlipidaemic rats

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• 作者：Long-Yan Zhao^a ; ^b ; ¹ ; ^{zhaolongyan-dra@163.com}  ; [Author Vitae] ; Wei Huang^a ; ^b ; ¹ ; ^{348616542@qq.com} ; Qing-Xia Yuan^a ; ^b ; ^{qingxiayuan@163.com} ; Jie Cheng^a ; ^b ; ^{44431960@qq.com} ; Zhen-Chi Huang^a ; ^{zjyzhzc@163.com} ; Le-Jun Ouyang^a ; ^b ; ^{ouyanglejun@163.com} ; Fu-Hua Zeng^a ; ^{zengfuhua@gmail.com}
• 关键词：ODPs ; Opuntia dillenii Haw. polysaccharides ; ODP-Ia ; Opuntia dillenii Haw. polysaccharide-Ia ; TC ; total cholesterol ; TG ; triglyceride ; LDL-C ; low-density lipoprotein cholesterol ; VLDL-C ; very low-density lipoprotein cholesterol ; AI ; atherosclerosis index
• 刊名：Food Chemistry
• 出版年：2012
• 期刊代码：48_03088146
• 类别：abs
• 出版时间：15 September, 2012
• 卷：134
• 期：2
• 页码：964-971
• 文件大小：726 K

摘要

The antihyperlipidaemic effects of ODP-Ia, one of the main components of Opuntia dillenii Haw. polysaccharides, were studied. Gavage administration of ODP-Ia was observed to significantly decrease serum lipid levels and to increase serum high-density lipoprotein cholesterol level in hyperlipidaemic rats. Similar suppressive patterns were also seen in hepatic total cholesterol and triglyceride levels. Moreover, the ODP-Ia administration significantly increased serum lecithin:cholesterol acyltransferase activity, increased the production of serum NO, inhibited hepatic HMG-CoA reductase activity, augmented serum and hepatic superoxide dismutase activities and decreased the serum and hepatic malondialdehyde contents in hyperlipidaemic rats. In addition, a histopathological examination revealed that ODP-Ia administration significantly suppressed inflammatory cell infiltration and the expression of VCAM-1. Together, these results indicate that ODP-Ia is a potential natural product for the treatment of hyperlipidaemia-related diseases by improving antioxidant levels, modulating the activities of enzymes involved in cholesterol metabolism, promoting the production of NO and suppressing the expression of VCAM-1, thereby suppressing lipid accumulation and inflammatory cell infiltration.