【摘要】 目的　进一步探讨环孢素A(CsA)肾毒性的发病机制 ,并为临床防治CsA所致急性肾损伤提供依据。方法　采用生化、免疫组化和透射电镜方法。结果　CsA使肾皮质内皮素 - 1(ET - 1)水平增高 ,肾组织中超氧化物歧化酶 (SOD)活力下降 ,丙二醛 (MDA)含量增多 ,肾小管上皮细胞Na+ ,K+ -ATP酶活性降低 ,并造成肾、肝、肺组织结构破坏 ,还原性谷胱甘肽 (TAD)可使上述病变减轻。结论　血流动力学改变和脂质过氧化损伤是CsA致急性肾损伤的重要原因 ,TAD有良好的保护作用。更多还原

【Abstract】 Objective To investigate the mechanism of cyclosporin A(CsA) nephrotoxicity and to provide the evidence for prevention and treatment of acute renal injury induced by CsA. Methods Biochemical method, immunohistochemical method and electron microscope were used to determine the changes of endothelin-1(ET-1) level, malondialdehyde (MDA) and superoxide dismutase (SOD) content, and Na +, K +-ATP ase activity. Pathological findings were also observed.Results CsA caused remarkably increases of ET-1 level and MDA content, but the activities of SOD and Na +, K +-ATP ase decreased significantly. The structural damages in kidney, liver, and lung were also seen. Reduced glutathione (TAD) could relieve these changes. Conclusion The change of renal hemodynamics and the lipid peroxidation was important causes of acute renal injury induced by CsA. TAD could play a protective role.更多还原