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目的研究环孢素Ａ（ＣｓＡ）的肾毒性机制。方法制备了体外ＣｓＡ致肾小管上皮细胞（ＴＥＣ）损伤模型，对ＴＥＣ内氨基酸组成、含量、ＡＴＰ水平及乳酸脱氢酶（ＬＤＨ）释放率等指标进行了一系列检测。结果（１）经ＣｓＡ处理，ＴＥＣ内氨基酸水平没有明显变化；（２）体外投入甘、丙氨酸对ＣｓＡ所致的损伤可起保护作用，其作用与投入时机及剂量有关，而与Ｎａ＋－Ｋ＋－ＡＴＰ酶的抑制无直接联系。结论ＣｓＡ肾中毒时对细胞内氨基酸代谢影响不大，甘、丙氨酸对ＣｓＡ性肾损伤有明确的保护作用，其作用发挥可不依赖正常的能量代谢
Objective To study the nephrotoxicity mechanism of CsA. Methods The injury model of tubular epithelial cells (TEC) induced by CsA in vitro was established. A series of tests were carried out on the content of amino acid, the content of ATP, the level of ATP and the release rate of lactate dehydrogenase (LDH) in TEC. Results (1) There was no significant change of amino acid level in TEC after CsA treatment. (2) Glycine and alanine could protect CsA - induced injury in vitro, K + -ATP enzyme inhibition is not directly related. Conclusions CsA nephrotoxicity has little effect on intracellular amino acid metabolism. Glycyrrhizinate and alanine have clear protective effects on CsA-induced renal injury, and their effects can be independent of normal energy metabolism