高级检索
张敬, 谭莉丽, 张军, 石红军. 镍化合物对大鼠肺泡巨噬细胞凋亡影响[J]. 中国公共卫生, 2009, 25(3): 361-362. DOI: 10.11847/zgggws2009-25-03-56
引用本文: 张敬, 谭莉丽, 张军, 石红军. 镍化合物对大鼠肺泡巨噬细胞凋亡影响[J]. 中国公共卫生, 2009, 25(3): 361-362. DOI: 10.11847/zgggws2009-25-03-56
shu
ZHANG Jing, TAN Li-li, ZHANG Jun, . Effect of nickel compounds on apoptosis of alveolar macrophages in rats[J]. Chinese Journal of Public Health, 2009, 25(3): 361-362. DOI: 10.11847/zgggws2009-25-03-56
Citation: ZHANG Jing, TAN Li-li, ZHANG Jun, . Effect of nickel compounds on apoptosis of alveolar macrophages in rats[J]. Chinese Journal of Public Health, 2009, 25(3): 361-362. DOI: 10.11847/zgggws2009-25-03-56
shu

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

    摘要
  • 摘要: 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。

     

    Abstract: Objective To explore the mechanism of apoptosis of alveolar macrophages induced by nickel compounds.Methods Rats were treated with Ni3S2 and Ni2O3.Sixteen months later,pulmonary alveolar macrophages(AM)of all experimental rats were collected.Apoptosis of AM was measured by propid iumstaining 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).Conclusion Changes of intracellular calcium and mitochondrial membrane electric potential may play pivotal roles in apoptosis of AM induced by nickel.

     

    • HTML全文
    • 参考文献(0)
    • 相关文章
    • 施引文献
  • 资源附件(0)

/

返回文章
返回