IL-6影响骨髓基质细胞凋亡机理的初步探讨

目的通过观察IL-6对体外培养骨髓基质细胞凋亡的影响，探讨骨髓基质细胞凋亡的机理。方法取1月龄SD大鼠的骨髓基质细胞进行体外培养，通过透射电子显微镜观察、bax、bcl-2蛋白免疫组化染色、流式细胞仪检测凋亡细胞周期变化及线粒体跨膜电位改变、RT—PCR法检测凋亡细胞bax、bcl-2 mRNA表达等指标进行观察。结果IL-6组细胞G1期、凋亡率和线粒体膜电位改变均非常显著高于对照组；随着诱导时间的延长，Bcl-2 mRNA表达呈逐渐下降趋势，BaxmRNA表达呈逐渐升高趋势。Bcl-2／Bax：随着诱导时间的延长呈下降趋势。结论IL-6使大量细胞停留在G1期，阻滞细胞进入S期，使DNA合成受阻；IL-6促进凋亡的作用是通过1促进bax从胞浆中移至线粒体膜上而使bax在与bcl-2形成的异二聚体中占据优势来促进线粒体上的PT孔道开放，使内膜离子通道改变，线粒体内膜电位下降或丧失，导致Cyto c等蛋白的释放来调节细胞凋亡。

Mechanism of IL-6 influencing apoptosis of marrow stromal cells

Objective To investing at the mechanism of the effect of IL-6 on apoptosis of marrow stromal cells in vitro. Methods Marrow stromal cells were separated from the extremties of 30-day SD rats in vitro. Cell ultrastructure was observed, flow cytometry was used for studying apoptotic cell cycle and mitochondrion membrane potential changes, immunohisto-chemistry for bcl-2 and bax protein, and RT-PCR for bax and bcl-2 mRNA expression of apoptotic cells. Results Cell cycle G1, rate of apoptosis, and mitochondrion membrane potential in IL-6 group were significantly higher than in control group. along with prolonging induction time, the expression of Bcl-2 mRNA gradually declined, and bax mRNA increased contrarily.Conclusions IL-6 increases the cells that are blocked at G1, stopping them from composing DNA. It promotes apoptosis by faciditating the transfer of bax protein from cyto plasm to mitochondrial membrane so that bax predominates in the dimer formed by bax and bcl-2;precipitating opening of permeability transforming pores of mitochondria, change in channels of nito chondrial, inner membrane and dropor loss of mitochondrial membrane potential, leading to relense of cyto c and other profeins to regnlate cell apoptosis.