The analysis of the function of PPARγin endothelium on the attenuation of the diabetic vascular disease using PPARγendothelium specific deficient mice.

合成的ppar γ配体为改善脂肪细胞分化相关的胰岛素抵抗提供了证据。合成ppar γ配体对血管系统的有效作用已有报道，但其作用机制尚不清楚。为了研究内皮细胞中PPARγ表达在糖尿病血管疾病过程中的作用，我们对内皮细胞特异性PPARγ敲除（PPARγ）进行了研究。制备E-null小鼠。PPARγ。与对照组PPARγ相比，饲喂高脂肪饮食的E-null小鼠的收缩压明显升高。E-wild老鼠。高脂饮食处理后PPARγ主动脉中Egr-1、il -1β和IL-6的表达水平。与PPARγ相比，E-null小鼠升高。E-wild老鼠。PPARγ。饲喂高脂饲料的E-null小鼠的葡萄糖水平升高，肝脏脂肪堆积减少，而PPARγ。与PPARγ相比，E-null小鼠血清甘油三酯浓度和游离脂肪脂水平较高。E-wild老鼠。PPARγ。与apoe敲除小鼠杂交后，高脂饲料喂养的小鼠动脉粥样硬化发生加速，但PPARγ对主动脉动脉粥样硬化区发生率无显著影响。e -null apoe KO和PPARγ。野生apoe KO小鼠。本研究证实内皮细胞中表达的ppar γ对apoe敲除小鼠的炎症和脂质代谢有调节作用，而内皮细胞中表达的ppar γ对apoe敲除小鼠动脉粥样硬化的进展无显著影响。

The synthetic PPARγligands have provided the evidence with the improvement of insulin resistance associated with adipocyte differentiation. The effective role of synthetic PPARγligands on vascular system has been reported, but the mechanism has not been clear. To study the role of PPARγexpressed in endothelial cell on the process of diabetic vascular disease, the endothelial cell specific PPARγknock out(PPARγ. E-null) mice were produced. PPARγ. E-null mice fed with high fat diet had significantly elevated systolic blood pressure compared with control PPARγ. E-wild mice. After high fat diet treatment the expression levels of Egr-1, IL-1βand IL-6 in the aorta of PPARγ. E-null mice were elevated compared with PPARγ. E-wild mice. PPARγ. E-null mice fed high fat diet showed the improvement of elevated glucose level and fewer fat accumulation in liver whereas PPARγ. E-null mice showed higher concentration of serum triglyceride and free fatty lipid levels compared with PPARγ. E-wild mice. PPARγ. E-null crossed with apoe knock out mice fed with high fat diet showed accelerated atherogenesis, but there was no significant difference in the rate of atherosclerotic region in aorta between PPARγ. E-null-apoe KO and PPARγ. wild-apoe KO mice. In this study it is proved that PPARγexpressed in endothelial cell regulates inflammation and lipid metabolism whereas PPARγexpressed in endothelial cell has no significant effect on the progression of atherogenesis in apoe knock out mice.