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作为新一代的免疫抑制剂,环孢素(Cy-closporine,以下简称CsA)开创了人类器官移植等领域免疫抑制治疗的新纪元,但它同时产生的明显肾功能损害,则严重地限制了它的广泛应用。因此,明确CsA的肾毒作用机制,并找到预防或缓解CsA肾毒的有效方法,就成为近年来人们普遍关心的课题。本文仅就目前对CsA肾毒作用机制的认识和研究现状作一简要综述。一、CsA肾毒的原发作用部位总的来说,CsA肾毒作用的机制仍不明确。最初的临床和动物实验研究,基于近曲小管上皮细胞和肾间质结构与功能的改变,认为CsA本身是一种直接的肾毒剂。但是,由于CsA引起的肾小管的组织学变化并不是独一无二的,
As a new generation of immunosuppressant, Cy-closporine (hereinafter referred to as CsA) has opened up a new era of immunosuppressive therapy in the field of human organ transplantation. However, its obvious simultaneous impairment of renal function severely limits its widely used. Therefore, to clarify the renal nephrotoxicity mechanism of CsA and to find an effective way to prevent or relieve CsA nephrotoxicity has become a topic of general concern in recent years. This article only on the current mechanism of CsA nephrotoxicity understanding and research status to make a brief review. First, the main role of CsA nephrotoxicity site In general, the mechanism of CsA nephrotoxic effect is still not clear. Initial clinical and animal experimental studies, based on changes in the structure and function of proximal tubule epithelial cells and renal interstitium, suggest that CsA itself is a direct nephrotoxic agent. However, due to the histological changes of renal tubules caused by CsA is not unique,