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作 者:范春雷[1] 高丽萍[1] 沃兴德[1] 严瑾 宋家梁[1]
机构地区:[1]浙江中医学院生命科学系,浙江杭州310053
出 处:《中国药理学通报》2005年第6期746-751,共6页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No30070932)
摘 要:目的研究川芎嗪对SRAI基因表达的影响,从基因调控水平探讨其抗动脉粥样硬化作用的机制。方法将人SRAI基因构建在γ干扰素活性位点(GAS)调控元件的下游,并导入爪蟾卵母细胞,建立人类清道夫受体SRAI基因表达调控系统。分别用经oxLDL刺激培养牛主动脉平滑肌细胞后制备的平滑肌细胞条件培养液(SCM)以及含有川芎嗪的SCM培养卵母细胞。3d后,对卵母细胞膜上的SRA1表达量检测。结果结果显示川芎嗪可抑制SCM诱导的SRAI表达,且有量效关系。结论说明川芎嗪和γ干扰素有类似的作用,可以通过干预GAS调控途经,阻止oxLDL诱导引起的SRA1过量表达。Aim To investigate and evaluate the effect of ligustrazine on the expression of scavenger receptor type AI, the human γ-interferon activation site (GAS) elements regulatory systems of SR-AI expression wasfirst established in the Xenopus oocytes. Methods A plasmid, in which the human SR-AI gene was constructed downstream from the GAS elements, was microinjected into the nucleus of Xenopus oocytes. The oocytes then were cultured in the smooth muscle cell conditioned medium (SCM), In which the cell were cultured with the treatment of oxLDL for 2 days. In the other groups, the oocytes were treated with SCM containing the nature medicines ligustrazine, and the positive control drug γ-interferon respectively. Results The results demonstrated that SCM could upregulate the expression of SR-AI in this system, this action was suppressed by ligustrazine and γ-interferon. Conclusion Similar to the action of γ-interferon, ligustrazine can prevent the over-expression of SR-A induced by oxLDL, via their effect on the GAS elements regulatory pathway.
关 键 词:爪蟾卵母细胞 清道夫受体 γ-干扰素活性位点元件 氧化低密度脂蛋白 川芎嗪
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