Chen Xiao-Ling, Huang Shan-Sheng, Liu Kun, Ai Jie
Department of Pathophysiology, Institute of Basic Medical Sciences, Hebei Medical University, Shijiazhuang 050017, China.
Sheng Li Xue Bao. 2005 Oct 25;57(5):619-26.
To investigate the modulatory action of endogenous and exogenous nitric oxide (NO) on survival of alveolar macrophages (AMs) in different cellular states, AMs from normal rats (normal AMs) and from bleomycin (BLM)-treated rats (BLM AMs) were incubated by sodium nitroprusside (SNP, NO donor) and L-arginin (L-Arg, NO precursor), respectively. The survival of AMs was evaluated by apoptosis and cell cycles. The molecular mechanisms were investigated by the contents of Bcl-2, Bax proteins in AMs. The results are as follows: (1) The degree of BLM AMs apoptosis was higher than that of normal AMs; the number of BLM AMs in G(0)/G(1) phases was less than that of normal AMs; there was no significant difference in S+G(2)M phases between the number of BLM AMs and that of normal AMs. (2) Down-regulation of Bcl-2 and up-regulation of Bax occurred in BLM AMs, compared to those in normal AMs. (3) Apoptosis of AMs, either normal AMs or BLM AMs, was induced by both SNP and L-Arg, when compared to their respective control; only the number of BLM AMs in S+G(2)M phases was increased by L-Arg. (4) SNP and L-Arg induced a down-regulation of Bcl-2 and an up-regulation of Bax proteins in normal AMs, but did not induce the same change pattern in BLM AMs. (5) The Bax in BLM AMs was down-regulated by L-Arg. It is concluded that NO can induce the apoptosis of BLM AMs and normal AMs; that Bcl-2 and Bax are implicated in NO-induced apoptosis of normal AMs, whereas they are not involved in that of BLM AMs, suggesting the differential molecular mechanisms underlying the NO-induced apoptosis of normal AMs and BLM AMs; and that endogenous NO promotes proliferation of BLM AMs, which might be associated with down-regulation of Bax.
为研究内源性和外源性一氧化氮（NO）对不同细胞状态下肺泡巨噬细胞（AMs）存活的调节作用，分别用硝普钠（SNP，NO供体）和L-精氨酸（L-Arg，NO前体）孵育正常大鼠的AMs（正常AMs）和博来霉素（BLM）处理大鼠的AMs（BLM AMs）。通过凋亡和细胞周期评估AMs的存活情况。通过AMs中Bcl-2、Bax蛋白含量研究分子机制。结果如下：（1）BLM AMs的凋亡程度高于正常AMs；BLM AMs处于G(0)/G(1)期的细胞数量少于正常AMs；BLM AMs和正常AMs处于S+G(2)M期的细胞数量无显著差异。（2）与正常AMs相比，BLM AMs中Bcl-2下调，Bax上调。（3）与各自对照组相比，SNP和L-Arg均诱导正常AMs和BLM AMs凋亡；仅L-Arg增加了BLM AMs处于S+G(2)M期的细胞数量。（4）SNP和L-Arg诱导正常AMs中Bcl-2下调、Bax蛋白上调，但在BLM AMs中未诱导出相同的变化模式。（5）L-Arg使BLM AMs中的Bax下调。结论为，NO可诱导BLM AMs和正常AMs凋亡；Bcl-2和Bax参与NO诱导的正常AMs凋亡，而不参与BLM AMs凋亡，提示NO诱导正常AMs和BLM AMs凋亡的分子机制不同；内源性NO促进BLM AMs增殖，这可能与Bax下调有关。
