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Effects of advanced glycation end products on the survival and the morphology of bovine retinal endothelial cells and pericytes
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF OCULAR FUNDUS DISEASES
- Issue:
- 1
- DOI:
- 10.3760/j.issn:1005-1015.2006.01.004
- Key Word:
- 糖基化终末产物,高级;细胞培养;周细胞;血管内膜
Abstract： 目的观察体外孵育的牛血清白蛋白(BSA)非酶促糖基化终末产物(AGEs)对牛视网膜微血管内皮细胞(BREC)和周细胞(BRP)存活和形态的影响.方法取终浓度为50 mg/ml的牛血清白蛋白(BSA)、500 mmol/L D-葡萄糖,于37℃孵箱内避光孵育12周,制备外源性AGEs-BSA,经SephacrylS 300层析纯化,十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)蛋白电泳鉴定AGEs-BSA和coomassie蛋白质定量法测定蛋白浓度.分设不同浓度梯度的AGEs-BSA实验组和BSA对照组,以及空白对照组,分别观察体外孵育的AGEs-BSA对体外培养的BREC和BRP的毒性作用.相差倒置显微镜观察500μg/ml AGEs-BSA和BSA作用48 h对BREC和BRP形态的影响.结果随着AGEs-BSA剂量的增加,细胞被抑制呈上升趋势.500μg/ml AGEs-BSA抑制BREC为空白对照组的(72.8±15.9)%,抑制周细胞为空白对照组的(64.8±9.0)%.低浓度AGEs-BSA对BREC有一定促增生作用,但与空白对照组比较无统计学意义(P=0.231).相差倒置显微镜观察结果显示AGEs-BSA处理组细胞增殖受抑制,失去正常细胞形态,而BSA对照组细胞同空白对照组,细胞形态正常.结论AGEs-BSA在高浓度时,无论是对BREC还是BRP,都产生生长抑制作用,从而导致BRP的丢失,损伤血管功能.进一步证实了非酶糖化是糖尿病微血管并发症的一个重要原因.
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