Effect of Activation Leukocyte and Change of Leucocyte Medium on Hyperlipidemia and Blood Stasis Animal Model Induced by Immune Damaging and Stress
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    Abstract:

    Aim To establish a new animal model which is more suitable for the study on atherosclerosis and to investigate its mechanisms and to study the immunological and inflammtional mechanisms in the pathogenesis of atherosclerosis. Methods 40 Wistar rats were randomly divided into 4 groups. Rats of the first group (n=10) were fed with high cholesterol diet (HCD). Rats of the second group (n=10) were fed with high cholesterol diet and injected with xenoma serum protein (HCD XSP). Rats of the third group (n=10) were fed with high cholesterol diet and injected with xenoma serum protein and adrenine (HCD XSP A), rats of the forth group (n=10) were fed with normal diet and just injected with adrenine (ND A). The changes of platelet function, lipid metabolism, leucocyte activation and adhesiveness, mediators of inflammation and blood vessel endothelial function were observed in four groups. Results In comparison with the ND A group, TC and LDLC of the HCD XSP A group rised significantly (p<0.01). As to the interleukins, the three groups fed with high cholesterol diet had high level of IL 6 and the HCD and HCD XSP groups had high level of IL 8, compared with the ND A group (p<0.01). But in all of the four groups, IL 2 did not have marked difference. The ND A group had the high leukocyte adhesion molecule express rate (CD11/CD18) than the other three groups (p<0.05). Conclutions The hyperlipidemia model induced by combined facters (HCD XSP A) is more suitable for the study on atherosclerosis and its mechanisms of traditional Chinese medicine treatment. And the immunological and inflammtional mechanisms play an important role in the pathogenesis of atherosclerosis.

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ZHANG Hong Xia, LIU Jian Gang, MA Lu Bo,,SHI Da Zhuo. Effect of Activation Leukocyte and Change of Leucocyte Medium on Hyperlipidemia and Blood Stasis Animal Model Induced by Immune Damaging and Stress[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2003,11(2):99-102.

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History
  • Received:July 02,2002
  • Revised:December 16,2002
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