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机构地区:[1]洛阳东方医院,河南洛阳471003 [2]华中科技大学同济医学院
出 处:《河南科技大学学报(医学版)》2006年第3期166-168,共3页Journal of Henan University of Science & Technology:Medical Science
摘 要:目的 探讨脱氢表雄酮(DHEA)对氧化低密度脂蛋白诱导的血管平滑肌细胞中VCAM-1及MCP-1表达的影响,研究脱氢表雄酮在动脉粥样硬化中的作用。方法 取4~6周龄雄性SD大鼠,进行血管平滑肌细胞的原代培养,当细胞纯度达95%以上,取第3~4代细胞用于实验。按实验设计将培养细胞分为4个组:①正常对照组;②ox-LDL刺激组;③ox-LDL+DHEA组;④DHEA组。采用逆转录聚合酶链反应(RT-PCR)检测其VCAM-1及MCP-1mRNA的表达情况。结果 逆转录聚合酶链反应结果显示,各组细胞均表达VCAM-1mRNA和MCP-1mRNA,OX-LDL组VSMC表达的VCAM-1和MCP-1mRNA明显高于正常对照组(P〈0.01),而同时加入DHEA后其mRNA表达则有下降(P〈0.05及P〈0.01)。单独加DHEA组与正常对照组比较,VCAM-1和MCP-1mRNA表达与正常组mRNA无差异。结论 OX-LDL能明显诱导VSMC中VCAM-1及MCP-1的表达,DHEA能够抑制OX-LDL诱导的VSMC细胞VCAM-1及MCP-1的分泌,可能是其抗动脉粥样硬化的机制之一。Objective To investigate the effects of dehydroepiandrosterone (DHEA)on expression of VCAM-1 and MCP-1 in vascular smooth muscle cells induced by oxidized low-density lipoprotein. To study the effects of dehydroepiandrosterone in atherosclerosis, the possible mechanism of its antiatherosclerosis. Methods Rat aortic SMCs were prepared from 4 ~ 6 week old SD rat. When the purity of cells achieved 95 %, the cells of the third or the fourth passage were used in experimentation. We separated the cells into four groups according to the experimental plan: ①control group; ② ox-LDL stimulated group; ③ox-LDL + DHEA group; ④DHEA group. The expression of VCAM-1 and MCP-1 mRNA were determined by semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR). Results RT-PCR showed that VCAM-1 and MCP-1 mRNA was expressed in all groups. Higher level of VCAM-1 and MCP-1 mRNA expression induced by ox-LDL was observed in ox-LDL stimulated group compared with that in control group( P 〈 0.01 ). After being treated with dchydroepiandrosterone, the expression of VCAM-1 and MCP-1 mRNA in ox-LDL + DHEA group was reduced( P 〈 0.05 and P 〈 0.01 ). The expression of VCAM-1 and MCP-1 mRNA of DHEA group had no distinctive difference compared with control group. Conclusion The mRNA in cultured VSMC is markedly induced by ox-LDL, and the expressions of VCAM-1 and MCP-1 protein and mRNA induced by ox-LDL can be inhibited by dehydroepiandrosterone. That may be one of the mechanisms of antiatherosclerotic effect of DHEA.
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