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目的：研究马兜铃酸Ｉ（ＡＡＩ） 所致ＬＬＣＰＫ１ 细胞凋亡时细胞内游离钙离子浓度（［ Ｃａ２＋ ］ｉ） 的变化和钙拮抗剂拉西地平对细胞凋亡的作用。 方法：应用已建立的ＡＡＩ 所致ＬＬＣＰＫ１ 细胞凋亡模型，使用光镜、ＡｎｎｅｘｉｎＶＦｌｕｏｓ 凋亡检测试剂盒和流式细胞仪检测细胞凋亡，经Ｆｌｕｏ３／ＡＭ 染色，激光扫描共聚焦显微镜测定平均［Ｃａ２＋］ｉ 。 结果：０－０４ ｇ／Ｌ 的ＡＡＩ 作用２４ｈ 可致ＬＬＣＰＫ１ 细胞出现明显细胞凋亡和平均［Ｃａ２＋］ｉ 显著升高；拉西地平（１００ ｎｇ／Ｌ，１ μｇ／Ｌ） 可显著抑制ＡＡＩ 所致的［Ｃａ２ ＋］ｉ 升高并能降低凋亡细胞比例。 结论：在体外条件下ＡＡＩ 所致ＬＬＣＰＫ１ 细胞凋亡的发生可能与［Ｃａ２＋］ｉ 升高有关；拉西地平可能通过抑制［ Ｃａ２＋］ｉ 升高而抑制ＡＡＩ 所致的凋亡。
OBJECTIVE: To study the changes of intracellular free calcium concentration ([Ca2 +] i) and the effect of laccipine on apoptosis in LLCK1 cells induced by aristolochic acid I (AAI). Methods: The apoptosis model of LLCPK1 cells induced by AAI was established. Apoptosis was detected by light microscopy, AnnexinVFluos apoptosis detection kit and flow cytometry. Fluo3 / AM staining , Laser scanning confocal microscopy to determine the average [Ca2 +] i. Results: Apoptosis of LLCK1 cells induced by 0-04 g / L AAI for 24 h resulted in a significant increase of average [Ca2 +] i. Laxidipine (100 ng / L, 1 μg / L) AAI-induced [Ca2 +] i increase and can reduce the proportion of apoptotic cells. Conclusions: The apoptosis of LLC-PK1 cells induced by AA may be related to the increase of [Ca2 +] i induced by AAI in vitro. Lacidipine may inhibit AAI-induced apoptosis by inhibiting the increase of [Ca2 +] i.