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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。
Apoptosis morphologically manifested as chromatin condensation, the biochemical performance of nuclease digestion DNA. This study attempted to investigate the mechanism of endotoxin (lipopolysaccharide) -induced apoptosis in murine peritoneal macrophages. The results showed that endotoxin induced the apoptosis of macrophages, and compared with the control group, the phagocytic function of cells was significantly decreased (P <0.01). The concentration of NO-2 / NO-3 in peritoneal lavage fluid was significantly increased. Both NO inhibitor and PDTC could partially inhibit macrophage apoptosis and partial phagocytosis. Using LPS and IFN to simulate in vivo conditions, apoptosis of cultured macrophages can also be induced. Similar to the overall situation, AG and PDTC also partially inhibited mouse macrophage apoptosis. Tip endotoxin-induced mouse peritoneal macrophage apoptosis by NO and reactive oxygen species mediated.