脉心康对平滑肌细胞源性泡沫细胞过氧化体增殖物激活型受体γ与腺苷三磷酸结合盒转运体1 mRNA表达的影响

目的 观察脉心康干预大鼠血管平滑肌细胞源性泡沫细胞中过氧化体增殖物激活型受体γ、腺苷三磷酸结合盒转运体A1(ABCA1)mRNA表达变化,以探讨脉心康对动脉粥样硬化泡沫化细胞形成的可能调控机制.方法 用组织块培养法培养大鼠血管平滑肌细胞,以氧化型低密度脂蛋白使其泡沫化,并以脉心康、罗格列酮分别干预.采用原位杂交技术观察过氧化体增殖物激活型受体γ、腺苷三磷酸结合盒转运体A1 mRNA表达变化.结果 脉心康与罗格列酮均能提高过氧化体增殖物激活型受体γ、腺苷三磷酸结合盒转运体A1 mRNA表迭,与生理盐水组、空白对照组相比,均有显著性差异(P<0.01),脉心康组优于罗格列酮组(P<0.01).结论 脉心康具有与罗格列酮相似的过氧化体增殖物激活型受体γ激动作用,且优于罗格列酮.其抗动脉粥样硬化作用的分子机制与过氧化体增殖物激活型受体γ调控途径有关,有望成为中医药领域中新的、特异性较高的过氧化体增殖物激活型受体γ激动剂,为抗动脉粥样硬化和脂代谢异常提供更佳的药物选择.

Effect of Maixinkang on PPARγ, and ABCA1 mRNA in Vascular Smooth Muscle Cells-derived Foam Cells in Rats

Aim To investigate the effect of Maixinkang on peroxisome proliferators-activated receptor γ (PPARγ) and ATP-binding cassette transporter A1 (ABCA1) in vascular smooth muscle cells (VSMCs) derived foam cells, to approach Maixinkang possible regulation mechanism for artherosclerosis (As) foam cells. Methods The cultured VSMCs were loaded with oxidized low density lipoprotein (ox-LDL) and intervened by Maixinkang and Rosiglitazone. The expressions of PPARγ and ABCA1 mRNA were detected with hybridization in situ.Results Maixinkang and Rosiglitazone could raise PPARγand ABCA1 mRNA, which were significant different to that in the isotonic Na chloride group and the blank group. Moreover, Maixinkang had difference with Rosiglitazone. Conclusions Maixinkang have effect of exciting PPARγ (P < 0.01), it is surpass to Roaiglitazone (P < 0.01). The molecule mechanism of anti-atherosclerosis is related with the channel of regulating PPARγ. As a new and higher specificity PPARγ excitomotory, Maixinkang is anticipated to supply more effective treatments for anti-atheresclerosis and lipid anomal-metabolism.