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

被引:84
|
作者
Zhao, Long-Yan [1 ,2 ]
Huang, Wei [1 ,2 ]
Yuan, Qing-Xia [1 ,2 ]
Cheng, Jie [1 ,2 ]
Huang, Zhen-Chi [1 ]
Ouyang, Le-Jun [1 ,2 ]
Zeng, Fu-Hua [1 ]
机构
[1] Zhanjiang Normal Univ, Coll Life Sci & Technol, Zhanjiang 524048, Guangdong, Peoples R China
[2] Hunan Agr Univ, Coll Biol Sci & Technol, Changsha 410128, Hunan, Peoples R China
关键词
Opuntia dillenii Haw; Polysaccharide; Hyperlipidaemia; Artherosclerosis; NITRIC-OXIDE SYNTHASE; LIVER-DISEASE; ATHEROSCLEROSIS; PEROXIDATION; EXPRESSION; OBESITY; MICE;
D O I
10.1016/j.foodchem.2012.03.001
中图分类号
O69 [应用化学];
学科分类号
081704 ;
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. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:964 / 971
页数:8
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