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首页> 外文期刊>Endocrinology >Vitamin D Prevents Podocyte Injury via Regulation of Macrophage M1/M2 Phenotype in Diabetic Nephropathy Rats
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Vitamin D Prevents Podocyte Injury via Regulation of Macrophage M1/M2 Phenotype in Diabetic Nephropathy Rats

机译：维生素D通过调节糖尿病肾病大鼠巨噬细胞M1 / M2表型防止足细胞损伤

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Increasing evidence suggests the heterogeneity of macrophage phenotype and function ultimately determines the outcome of diabetic nephropathy (DN). This study aimed to investigate the effects of vitamin D on macrophage M1/M2 phenotype and its role in preventing podocyte impairment in streptozotocin-induced DN rats. Calcitriol, a bioactive 1,25-dihydroxyvitamin D-3, ameliorated proteinuria and renal damage as well as reversed the decline of both nephrin and podocin, crucial structural proteins in podocytes. DN rats showed increased infiltrating macrophages with M1 phenotype characterized by elevated expression of inducible nitric oxide synthase and TNF-alpha in glomeruli and interstitium, which were inhibited after calcitriol treatment. Interestingly, calcitriol promoted M2 macrophage activation with enhanced expression of CD163, arginase-1, and mannose receptor at week 18 but not at week 8 or 14. The ratio of CD163 to CD68, considered as the proportion of M2 macrophages, was about 2.9-fold higher at week 18 after calcitriol treatment. Furthermore, the protein expression of inducible nitric oxide synthase, a crucial marker of M1 macrophages, was negatively correlated with the expression of either nephrin or podocin, whereas CD163, indicating M2 macrophages, was positively correlated. In vitro, 1,25-dihydroxyvitamin D3 switched high-glucose-induced M1 macrophages toward an M2 phenotype in either U937-derived macrophages or RAW264.7 cells. Our results suggest that vitamin D not only reduces macrophage infiltration and inhibits M1 macrophage activation but also enhances M2 macrophage phenotype to protect against podocyte injury.
机译：越来越多的证据表明巨噬细胞表型和功能的异质性最终决定了糖尿病性肾病（DN）的结果。本研究旨在探讨维生素D对巨噬细胞M1 / M2表型的影响及其在预防链脲佐菌素诱发的DN大鼠足细胞损伤中的作用。骨化三醇，一种具有生物活性的1,25-二羟基维生素D-3，改善了蛋白尿和肾脏损害，并逆转了nephrin和podocin（足细胞中的关键结构蛋白）的下降。 DN大鼠表现出M1型浸润性巨噬细胞增多，其特征是肾小球和间质中诱导型一氧化氮合酶和TNF-α的表达升高，而钙三醇治疗后可抑制这些表达。有趣的是，骨化三醇在第18周时增强了CD163，精氨酸酶-1和甘露糖受体的表达，从而促进了M2巨噬细胞的活化，但在第8周或第14周时却没有。CD163与CD68的比率（被视为M2巨噬细胞的比例）约为2.9-骨化三醇治疗后第18周的血红蛋白含量增加了三倍。此外，诱导型一氧化氮合酶的蛋白表达是M1巨噬细胞的关键标志，与nephrin或podocin的表达呈负相关，而指示M2巨噬细胞的CD163呈正相关。在体外，在U937衍生的巨噬细胞或RAW264.7细胞中，1,25-二羟基维生素D3将高糖诱导的M1巨噬细胞切换为M2表型。我们的结果表明，维生素D不仅可以减少巨噬细胞的浸润并抑制M1巨噬细胞的活化，还可以增强M2巨噬细胞的表型来保护足细胞免受损伤。

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