Chitosan increases the release of renal dipeptidase from porcine renal proximal tubule cells

H. Yoon, Y. H. Kim, Sung Wook Park, Hwanghee-Blaise Lee, H. Park
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引用次数: 2

Abstract

Renal dipeptidase (RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19) has been widely studied since it was first purified from porcine kidney brush border membrane. It was reported that RDPase activity in urine samples of acute and chronic renal failure patients decreases. Nitric oxide (NO) is a highly reactive free radical involved in a number of physiological and pathological processes. NO is able to act in a dual mode, leading either to induction of apoptosis or to blunted execution of programmed cell death. NO inhibited the RDPase release from porcine renal proximal tubules, which could be blocked by L‐NAME. Chitosan, the linear polymer of D‐glucosamine in β(1?4) linkage, not only reversed the decreased RDPase release by NO but also increased NO production in the proximal tubule cells. The stimulatory effect of NO on RDPase release from proximal tubules in the presence of chitosan must be different from the previously proposed mechanism of RDPase release via NO signaling pathway. Chitosan stimulated the RDPase release in the proximal tubules and increased RDPase activity to 220% and 250% at 0.1% and 1%, respectively. RDPase release was decreased to about 40% in the injured proximal tubules and was recovered in proportion to the increase of chitosan. Chitosan may be useful in recovery of renal function from HgCl2 injury.
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壳聚糖增加猪肾近端小管细胞肾二肽酶的释放
肾二肽酶(RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19)自首次从猪肾刷状缘膜中纯化得到以来,得到了广泛的研究。据报道,急性和慢性肾功能衰竭患者尿液样本中RDPase活性降低。一氧化氮(NO)是一种高活性自由基,参与许多生理和病理过程。NO能够以双重模式起作用,导致细胞凋亡的诱导或程序性细胞死亡的钝化。NO可抑制猪肾近端小管RDPase的释放,这一作用可被L‐NAME阻断。壳聚糖是β(1?4)链D -氨基葡萄糖的线性聚合物,它不仅逆转了RDPase释放的减少,而且增加了近端小管细胞中NO的产生。壳聚糖存在下,NO对近端小管RDPase释放的刺激作用一定不同于之前提出的RDPase通过NO信号通路释放的机制。壳聚糖刺激近端小管中RDPase的释放,在0.1%和1%的作用下,RDPase活性分别提高220%和250%。RDPase在损伤的近端小管中释放减少约40%,并与壳聚糖的增加成比例恢复。壳聚糖可能有助于盐酸损伤后肾功能的恢复。
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