PURPOSE:To clarify whether endogenous peroxisome proliferator-activated receptor gamma (PPARgamma) and its ligand, rosiglitazone, affect retinal leukostasis and the associated vascular leakage using an experimental diabetic model. METHODS:Diabetes was induced in heterozygous PPARgamma+/- mice and Brown Norway rats with an intraperitoneal streptozotocin (STZ) injection. Retinal leukostasis and leakage, quantified by concanavalin A (Con A) lectin perfusion labeling combined with a fluorophotometric dextran leakage assay, were investigated at 120 days in diabetic PPARgamma+/- and wild-type mice and at 21 days in diabetic rats receiving rosiglitazone or the vehicle. The retinal protein expression levels of vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF)-alpha, and the intercellular adhesion molecule (ICAM)-1 were investigated by means of the ELISA assay. RESULTS:In the diabetic PPARgamma+/- mice, retinal leukostasis and leakage were greater than in the diabetic wild-type mice. In addition retinal leukostasis and leakage were suppressed by treatment with rosiglitazone in experimental diabetic rats. ELISA analysis revealed that the upregulated ICAM-1 expression in the diabetic rat retina was reduced by rosiglitazone treatment. CONCLUSIONS:An endogenous pathway involving PPARgamma provides protection against retinal leukostasis and retinal leakage in diabetes and treatment with PPARgamma specific ligands inhibits retinal leukostasis and retinal leakage in diabetic rats.

译文

目的:使用实验性糖尿病模型来阐明内源性过氧化物酶体增殖物激活受体γ(PPARgamma)及其配体罗格列酮是否会影响视网膜白细胞形成和相关的血管渗漏。
方法:通过腹腔注射链脲佐菌素(STZ)在杂合性PPARγ/-小鼠和褐挪威大鼠中诱导糖尿病。通过伴刀豆球蛋白A(Con A)凝集素灌注标记结合荧光光度右旋糖酐泄漏测定定量研究视网膜白细胞的形成和渗漏,在糖尿病PPARγ/和野生型小鼠中在120天时以及在接受罗格列酮或糖尿病的糖尿病大鼠中在21天时进行了研究。车辆。 ELISA法检测了血管内皮生长因子(VEGF),肿瘤坏死因子(TNF)-α和细胞间黏附分子(ICAM)-1的视网膜蛋白表达水平。
结果:糖尿病PPARγ/-小鼠的视网膜白细胞增多和渗漏大于糖尿病野生型小鼠。此外,在实验性糖尿病大鼠中,通过罗格列酮治疗可抑制视网膜白细胞形成和渗漏。 ELISA分析显示,罗格列酮治疗可降低糖尿病大鼠视网膜中ICAM-1的表达。
结论:涉及PPARγ的内源性途径为糖尿病患者的视网膜白细胞增多和视网膜渗漏提供了保护,而PPARγ特定配体的治疗抑制了糖尿病大鼠的视网膜白细胞减少和视网膜渗漏。

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