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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(P<0.05),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(P<0.05),以及细胞凋亡蛋白cleaved caspase3的轻度增加,乳酸脱氢酶活性增加(P<0.05);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(P<0.05)。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。
Objective: To investigate the effect of albumin on tubulointerstitial injury induced by high glucose and its mechanism. Methods: The proximal tubular epithelial cell line NRK-52E was cultured in vitro and the changes of autophagy in high glucose culture were observed. Simultaneously, BSA alone was used to stimulate the renal tubular epithelial cells The expression of autophagy protein and the expression of apoptotic protein were observed. Then, low concentration of albumin was added into high glucose culture to observe the injury effect and autophagy of renal tubular epithelial cells. Results: The expression of autophagy protein Beclin-1 in renal tubular epithelial cells was increased under high glucose conditions (P <0.05), and the expression of Beclin-1 and Atg12 in renal tubular epithelial cells was also induced by low concentration of albumin (P <0.05) , And a slight increase of cleaved caspase3 and an increase of lactate dehydrogenase activity (P <0.05). However, a small amount of albumin inhibited the expressions of autophagy Beclin-1 and Atg12 in renal tubular epithelial cells , And significantly increased the expression of cleaved caspase3 (P <0.05). Conclusion: Autophagy is a protective mechanism of the cell itself. In the context of high glucose, albumin promotes the damage of the tubulointerstitium through its own regulatory mechanism that affects autophagy.