论文部分内容阅读
分别用一氧化氮(nitric oxide,NO)供体硝普钠(sodium nitroprusside,SNP)和前体L-精氨酸(L-arginin,L-Arg)孵育来自正 常大鼠(alveolar macrophages from normal rats,normal AMs)和滴注博莱霉素大鼠的肺泡巨噬细胞(alveolar macrophages from BLM-treated rats,BLM AMs),以探讨NO对不同状态细胞生存的调节。用凋亡和细胞周期评价细胞生存,细胞内Bcl-2 和Bax蛋白含量探讨其分子机制。结果如下:(1)BLM AMs的凋亡多于normal AMs;G0／G1期BLM AMs数少于normal AMs:S+G2M期BLM AMs数与相应的normal AMs数间的差异无统计学意义;(2)与normal AMs相比,BLM AMs内 Bcl-2下凋,Bax上调;(3)与相应的对照比,SNP和L-Arg能诱导normal AMs和BLM AMs凋亡;L-Arg仅能增加S+G2M 期BLM AMs数:(4)SNP和L-Arg诱导normal AMs内Bcl-2下调和Bax上调,但不能使BLM AMs内的Bcl-2和Bax发生 上述变化:(5)L-Arg下调BLM AMs内的Bax。上述结果显示:NO能诱导BLM AMs和normal AMs凋亡;Bcl-2和Bax 与NO诱导的normal AMs凋亡有关,而与NO诱导的BLM AMs的凋亡无关,提示NO诱导normal AMs和BLM AMs分 子机制不同;内源性NO促进BLM AMs增殖,这可能与其下调Bax有关。
The alveolar macrophages from normal rats (alveolar macrophages from normal rats) were incubated with nitric oxide (NO) donor sodium nitroprusside (SNP) and the precursor L-arginin (L-Arg) , normal AMs) and BLM-treated rats (BLM AMs) were instilled to investigate the regulation of NO on the survival of cells in different states. Apoptosis and cell cycle evaluation of cell survival, intracellular Bcl-2 and Bax protein content explore its molecular mechanism. The results were as follows: (1) BLM AMs had more apoptosis than normal AMs; BLM AMs in G0 / G1 were less than those in normal AMs: S + G2M. There was no significant difference between BLM AMs and corresponding normal AMs; 2) Bcl-2 down-regulated and Bax up-regulated in BLM AMs compared with normal AMs; (3) SNP and L-Arg induced apoptosis of normal AMs and BLM AMs compared with the corresponding control; L-Arg only increased (4) SNP and L-Arg induced the down-regulation of Bcl-2 and up-regulation of Bax in normal AMs, but failed to make the changes of Bcl-2 and Bax in BLM AMs. (5) L-Arg Down-regulate Bax in BLM AMs. The above results showed that NO could induce the apoptosis of BLM AMs and normal AMs; Bcl-2 and Bax were related to the NO-induced apoptosis of normal AMs, but not to the NO-induced apoptosis of BLM AMs, suggesting NO induced normal AMs and BLM AMs Different molecular mechanisms; endogenous NO promote BLM AMs proliferation, which may be related to its down-regulation of Bax.