M-CSF诱导MnSOD表达减轻RAW264.7细胞氧化损伤

为探讨巨噬细胞集落刺激因子（M－CSF）对单核巨噬细胞氧化损伤的保护作用,以富含M－CSF的小鼠L929细胞条件培养液（L929－CM）作为M－CSF来源,以小鼠巨噬细胞系RAW264．7为模型,从形态学上观察了M－CSF对叔丁基氢过氧化物（tbOOH)引起的RAW264。7细胞氧化损伤的保护作用;并采用酶活性测定、TR－PCR等方法,他M－CSF对RAW264．7细胞超氧化物歧化酶（SOD）活性及基因表达的影响。结果发现,M－CSF可以减轻tbOOH对RAW264．7细胞的氧化损伤;M－CSF可以提高细胞总SOD活性;M－CSF还可增强RAW264．7细胞MnSOD mRNA的表达,且这一诱导作用可被放线菌素D（actinomycinD)阻断。提示M－CSF可通过诱导细胞MnSOD表达而减轻RAW264．7细胞的氧化损伤。

Macrophage colony-stimulating factor protects RAW264.7 cells from oxidative injury through the induction of MnSOD expression

To show the protective effect of macrophage colony-stimulating factor (M-CSF) on macrophages under oxidative stress, we investigated the effect of M-CSF on RAW264.7 cells incubated with tert-butyl hydroperoxide (tbOOH) using L929 cell conditioned medium (L929-CM) as the source of M-CSF. The results showed that M-CSF could alleviate the tbOOH- induced oxidative injury to RAW264.7 cells. We also found that M-CSF could improve superoxide dismutase (SOD) activity in the cells. MnSOD mRNA expression was also shown to be increased by RT-PCR technique, and the induction could be blocked by actinomycin D. So,we concluded that M-CSF could protect RAW264.7 cells from oxidative injury through inducing MnSOD expression.