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MAO Junqin, HOU Zhonghai, CHEN Dagui, ZHANG Wen. Anti-hyperlipi-demic effects of polysaccharide MA from Mytilus coruscus on experimental atherosclerosis in rabbits[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(1): 27-30. doi: 10.3969/j.issn.1006-0111.2014.01.007
Citation: MAO Junqin, HOU Zhonghai, CHEN Dagui, ZHANG Wen. Anti-hyperlipi-demic effects of polysaccharide MA from Mytilus coruscus on experimental atherosclerosis in rabbits[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(1): 27-30. doi: 10.3969/j.issn.1006-0111.2014.01.007

Anti-hyperlipi-demic effects of polysaccharide MA from Mytilus coruscus on experimental atherosclerosis in rabbits

doi: 10.3969/j.issn.1006-0111.2014.01.007
  • Received Date: 2013-07-30
  • Rev Recd Date: 2013-09-14
  • Objective To explore the anti-hyperlipidemic effects and mechanism of polysaccharide MA from Mytilus coruscus in the experimental atherosclerosis rabbits and to observe the effects of MA on liver and aorta. Methods The atherosclerosis rabbit model was established by high-fat diet. The blood lipid such as triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL) in serum and enzymes metabolizing blood lipid such as lipoprteinlipase (LPL), hepaticlipase (HL) and hydroxymethylglutaryl CoA reductase (HMG-CoAR) were measured after atherosclerosis rabbits fed MA for 4 weeks. Histopathology and ultramicroscopic structure of hepatic tissue was observed. Lipid storage in aortic atherosclerotic plaque was observed by the oil red staining method. Results MA significantly reduced the level of TG, TC, LDL in serum and increased HL, LPL (P<0.05). MA reduced lipid storage in liver and aortic atherosclerotic plaque. Conclusion MA might play regulating effects in serum lipid by enhancing the activities of LPL and HL, and inhibit formation of atherosclerosis and fatty liver.
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    [6] 储智勇,毛俊琴,李铁军,等. 贻贝多糖对大鼠高脂血症的影响[J]. 解放军药学学报,2008,24(3):213-215.
    [7] 马明华,易杨华,汤海峰.厚壳贻贝多糖MA的分离纯化、理化性质及活性研究[J].中国海洋药物,2004, 4:14-18.
    [8] 李 玲,储智勇,袁 波,等.贻贝多糖胶囊辅助降血脂人体试食研究[J].中药材,2011,34(10):1645-1647.
    [9] 吴晓霞,李建科,刘迎利.蚕蛹油α-亚麻酸对实验性高血脂大鼠的降脂作用[J]. 食品科学,2011,32(15):285-288.
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    [11] 吴 涓,孙 倩,储智勇.贻贝多糖胶囊毒理学安全性研究[J]. 中国卫生检验杂志,2011,21(1):97-100.
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Anti-hyperlipi-demic effects of polysaccharide MA from Mytilus coruscus on experimental atherosclerosis in rabbits

doi: 10.3969/j.issn.1006-0111.2014.01.007

Abstract: Objective To explore the anti-hyperlipidemic effects and mechanism of polysaccharide MA from Mytilus coruscus in the experimental atherosclerosis rabbits and to observe the effects of MA on liver and aorta. Methods The atherosclerosis rabbit model was established by high-fat diet. The blood lipid such as triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL) in serum and enzymes metabolizing blood lipid such as lipoprteinlipase (LPL), hepaticlipase (HL) and hydroxymethylglutaryl CoA reductase (HMG-CoAR) were measured after atherosclerosis rabbits fed MA for 4 weeks. Histopathology and ultramicroscopic structure of hepatic tissue was observed. Lipid storage in aortic atherosclerotic plaque was observed by the oil red staining method. Results MA significantly reduced the level of TG, TC, LDL in serum and increased HL, LPL (P<0.05). MA reduced lipid storage in liver and aortic atherosclerotic plaque. Conclusion MA might play regulating effects in serum lipid by enhancing the activities of LPL and HL, and inhibit formation of atherosclerosis and fatty liver.

MAO Junqin, HOU Zhonghai, CHEN Dagui, ZHANG Wen. Anti-hyperlipi-demic effects of polysaccharide MA from Mytilus coruscus on experimental atherosclerosis in rabbits[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(1): 27-30. doi: 10.3969/j.issn.1006-0111.2014.01.007
Citation: MAO Junqin, HOU Zhonghai, CHEN Dagui, ZHANG Wen. Anti-hyperlipi-demic effects of polysaccharide MA from Mytilus coruscus on experimental atherosclerosis in rabbits[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(1): 27-30. doi: 10.3969/j.issn.1006-0111.2014.01.007
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