镍化合物对大鼠肺泡巨噬细胞凋亡影响

Effect of nickel compounds on apoptosis of alveolar macrophages in rats

目的研究镍化合物导致大鼠肺泡巨噬细胞凋亡机制。方法用Ni3S2和Ni2O3对大鼠进行染毒,16个月后收集各组动物的肺泡巨噬细胞,运用流式细胞术(FCM)测定细胞的周期分布、胞内钙离子浓度和线粒体膜电位。结果Ni3S2组大鼠肺泡巨噬细胞较对照组的凋亡率(%)明显增加〔(8.6±5.5)和(2.2±0.7),P<0.05〕,胞内游离钙浓度增加〔(26.6±8.7)和(19.5±0.5),P<0.05〕,线粒体膜电位变小〔(7.7±3.4)和(10.9±0.84),P<0.05〕。Ni2O3组较对照组的凋亡率和胞内游离钙浓度均增加,线粒体膜电位下降。结论线粒体膜电位下降,胞内外Ca2+浓度的改变可能是造成染镍大鼠肺泡巨噬细胞凋亡的原因。

Objective To explore the mechanism of apoptosis of alveolar macrophages induced by nickel compounds. Methods Rats were treated with Ni3 S2 and Ni20a. Sixteen months later, pulmonary alveolar macrophages （AM） of all experimental rats were collected. Apoptosis of AM was measured by propidium staining and flow cytometry （FCM）. Fluo-3 AM staining and FCM were used to detect the intracellular free calcium. Mitochondrial membrane electric potential was measured by rhodamine 123 staining with FCM. Results The apoptosis rate of AM in Ni3S2 treated rats （8. 6 ± 5. 5 ） was higher than that of control group （2. 2 ±0.7, P 〈 0. 05 ）. The intracellular calcium increased （26. 6 ± 8. 7 vs 19. 5 ± 0. 5, P 〈 0. 05 ） and mitochondrial membrane electric potential decreased（7. 7 ± 3.4 vs 10. 9 ± 0. 84, P 〈 0. 05 ）. Condusion Changes of intracellular calcium and mitochondrial membrane electric potential may play pivotal roles in apoptosis of AM induced by nickel.