内毒素诱导小鼠腹腔巨噬细胞凋亡的机制探讨

细胞凋亡在形态学上表现为染色质浓缩 ,生物化学上则表现为核酸酶酶切DNA。本研究试图探讨内毒素 (脂多糖 )诱导小鼠腹腔巨噬细胞凋亡的机制。结果显示 ,内毒素能诱导巨噬细胞凋亡 ,与对照组比 ,细胞吞噬机能显著下降 (P <0 .0 1) ,腹腔灌洗液中NO-2 /NO-3 浓度显著升高。NO阻断剂AG和活性氧阻断剂PDTC均能部分抑制巨噬细胞凋亡 ,细胞吞噬机能也获得部分恢复。用LPS和IFN模拟在体情况 ,也能诱导培养的巨噬细胞凋亡。与整体情况类似 ,AG和PDTC亦能部分抑制小鼠巨噬细胞凋亡。提示内毒素诱导小鼠腹腔巨噬细胞凋亡系经NO及活性氧介导.

The mechanism of macrophage apoptosis induced by lipopolysaccharide in mice

Apoptosis is a major form of cell death, characterized morphologically by chromatin condensation and biochemically by endonuclease cleavage of DNA into oligonucleosomal fragments. We investigated apoptosis mechanism of peritoneal macrophage(MΦ) induced by peritoneal injection of lipopolysaccharide(LPS) in mice. The results showed that: LPS induced the apoptosis of peritoneal MΦ and concomitant decrease of phagocytosis(vs control group, P<0.01), the concentration of NO - 2/NO - 3 in the peritoneal lavage fluid significantly increased after LPS injection; AG(inhibitor of iNOS) and PDTC(inhibitor of reactive oxygen species) prevented the apoptosis of MΦ and reduced the concentration of NO - 2/NO - 3 in the peritoneal lavage fluid. In vitro experiment, we found that AG and PDTC inhibited the apoptosis of MΦ induced by IFN(100?U·ml -1 ) +LPS (10?μg·ml -1 ) by using DNA gel electrophoresis analysis. These evidences support that NO and active oxygen species may be involved in the apoptosis process of peritoneal MΦ induced by LPS in mice.