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

使用 PPARγ 内皮特异性缺陷小鼠分析 PPARγ 在内皮细胞中对减轻糖尿病血管疾病的功能。

基本信息

批准号：
21591142
负责人：
ADACHI Masahiro
金额：
$ 2.91万
依托单位：
Kyushu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2009
资助国家：
日本
起止时间：
2009 至 2011
项目状态：
已结题

项目摘要

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.

人工合成的PPARγ配体为改善胰岛素抵抗和脂肪细胞分化提供了证据。人工合成的PPARγ配体对血管系统的作用已有报道，但其作用机制尚不清楚。为探讨内皮细胞表达的过氧化物酶体增殖物激活受体γ（PPARγ）在糖尿病血管病变过程中的作用，采用内皮细胞特异性过氧化物酶体增殖物激活受体γ基因敲除技术（endothelial cell specific PPARγknock out，PPARγ. E-null）小鼠。过氧化物酶体增殖物激活受体γ。与对照组相比，高脂饮食喂养的E-null小鼠的收缩压显著升高。野生老鼠高脂饲料处理后，Egr-1、IL-1β和IL-6在主动脉中的表达水平明显降低。E基因敲除小鼠与PPARγ相比升高。野生老鼠过氧化物酶体增殖物激活受体γ。E-null小鼠高脂饮食后血糖升高，肝脏脂肪堆积减少，而PPARγ则无明显变化。E-null小鼠的血清甘油三酯和游离脂肪水平高于PPARγ。野生老鼠过氧化物酶体增殖物激活受体γ。E-null与apoE基因敲除小鼠杂交后，高脂饮食可加速动脉粥样硬化的形成，而PPARγ与E-null杂交小鼠主动脉粥样硬化区形成率无显著性差异。E-null-apoe KO和PPARγ。野生型apoe KO小鼠。本研究证实，在apoE基因敲除小鼠中，内皮细胞表达的PPARγ调节炎症和脂质代谢，而内皮细胞表达的PPARγ对动脉粥样硬化的进展无明显影响。