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阐明肾小管上皮细胞损伤及再生过程中细胞凋亡的意义。方法：给Wistar大鼠腹腔注射庆大霉素，分别造成急性和慢性肾小管损伤模型，不同时间宰杀。用原位末端标记法及DNA琼脂糖凝胶电泳观察细胞凋亡，增殖细胞核抗原（PCNA）免疫组化观察增殖情况。将不同浓度的庆大霉素加入培养的大鼠肾小管上皮细胞诱导凋亡。结果：大剂量庆大霉素主要造成肾小管上皮细胞坏死，少量细胞凋亡。小剂量庆大霉素长时间作用以空泡变性、凋亡为主。各个时间点后者的凋亡细胞数均高于前者。肾小管上皮细胞第5天出现再生，第9天达高峰，细胞凋亡于第5天出现第一个高峰，第12天出现第二个高峰，发生于再生高峰之后。体外实验中，小剂量庆大霉素引起较多细胞凋亡，大剂量庆大霉素主要引起细胞坏死。结论：大剂量庆大霉素造成肾小管上皮损伤以坏死为主，小剂量庆大霉素造成肾小管上皮细胞损伤以变性、凋亡为主。凋亡在肾小管上皮细胞再生过程中，有重要的修饰和改建作用。
To clarify the significance of renal tubular epithelial cell injury and cell apoptosis during regeneration. Methods: The Wistar rats were injected intraperitoneally with gentamicin, which caused acute and chronic tubular injury models and killed at different times. Apoptosis was observed by in situ end labeling and DNA agarose gel electrophoresis. Proliferation of proliferating cell nuclear antigen (PCNA) was observed by immunohistochemistry. Different concentrations of gentamycin were added into cultured rat renal tubular epithelial cells to induce apoptosis. Results: Large doses of gentamicin caused necrosis of renal tubular epithelial cells and a small amount of apoptosis. Small doses of gentamicin for a long time to vacuolar degeneration, apoptosis-based. The latter at each time point the number of apoptotic cells were higher than the former. Renal tubular epithelial cells appeared to regenerate on the fifth day, reaching the peak on the ninth day, the first peak appeared on the fifth day and the second peak appeared on the twelfth day, which occurred after the peak of regeneration. In vitro experiments, a small dose of gentamycin caused more apoptosis, high doses of gentamicin caused cell necrosis. Conclusion: The high dose of gentamycin caused the necrosis of renal tubular epithelial cells, and the degeneration and apoptosis of renal tubular epithelial cells caused by low dose gentamicin. Apoptosis plays an important role in the regeneration of renal tubular epithelial cells.