高糖背景下白蛋白抑制肾小管上皮细胞的自噬表达

目的:探讨高糖背景下白蛋白造成肾小管间质损伤的作用及其机制。方法:体外培养大鼠近端肾小管上皮细胞系NRK-52E细胞,观察高糖培养环境下细胞自噬表达的改变;同时观察低浓度牛血清白蛋白(BSA)单独刺激,对肾小管上皮细胞自噬蛋白表达的影响以及细胞凋亡蛋白的表达改变;接着在高糖培养环境下加入低浓度的白蛋白刺激,观察肾小管上皮细胞的损伤效应及自噬表达情况。结果:高糖培养条件下肾小管上皮细胞自噬蛋白Beclin-1表达增加(P0.05),低浓度白蛋白也诱导肾小管上皮细胞自噬蛋白Beclin-1、Atg12表达增加(P0.05),以及细胞凋亡蛋白cleaved caspase3的轻度增加,乳酸脱氢酶活性增加(P0.05);但高糖培养下,少量白蛋白却抑制了肾小管上皮细胞自噬蛋白Beclin-1、Atg12的表达,并且显著增加了肾小管上皮细胞的凋亡蛋白cleaved caspase3的表达(P0.05)。结论:自噬是细胞自身的一种保护机制。在高糖背景下,白蛋白通过影响自噬的自身调节机制,促进了肾小管间质的损害作用。

Albumin Induced Autophagy Suppression of the Renal Tubular Epithelial Cells in High Glucose Media

Objective:To investigate the impact and mechanism of albumin induced renal epithelial cells injury.Methods:The cultured tubular epithelial cells were treated with bovine albumin or incubated with high glucose media, and their effects on autophagy and apoptosis were observed. Then after incubation with high glucose media the cells were treated with albumin, and the cell injury and autophagy changes were observed.Results:In the cultured tubular epithelial cells, autophagy was induced by high glucose while Beclin-1 expression was increased (P<0.05). Low density of BSA induced Beclin-1 highly expression in NRK-52E cells (P<0.05) while the decrease of apoptotic protein cleaved caspase3 was not obvious. But the cleaved caspase3 expression was increased largely induced by BSA in high glucose pre-treated cells (P<0.05), and Beclin-1, Atg12 expression was down-regulated at the same time.Conclusion:Autophagy acting as one of the cell self-protection mechanisms is inhibited by albumin which promoted renal tubular injury in the high glucose media.