CAJ | 학술논문

目的：探讨二硫化二砷诱导弥漫大 B 细胞淋巴瘤细胞株 LY8凋亡的机制。方法将不同浓度的二硫化二砷与弥漫大B细胞淋巴瘤细胞株LY8共培养。采用CCK-8方法测定细胞活性；AnnexinⅤ-PI方法测定细胞凋亡率，采用Western blot技术在蛋白水平测定凋亡相关因子BCL-2、Bax和caspase-3的表达。结果随着二硫化二砷浓度的增高，细胞活性越低，细胞凋亡率越高；随着二硫化二砷作用时间的延长，细胞活性越低，细胞凋亡率也越高。其差异均有统计学意义。Western blot结果显示：与对照组比较，二硫化二砷下调caspase-3蛋白的表达，Bax/BCL-2的比例升高并伴随着Bax断裂。结论二硫化二砷以时间和剂量依赖的方式抑制 LY8细胞生长和诱导凋亡，诱导凋亡的机制可能与线粒体通路相关，并伴随着Bax断裂。
목적：탐토이류화이신유도미만대 B 세포림파류세포주 LY8조망적궤제。방법장불동농도적이류화이신여미만대B세포림파류세포주LY8공배양。채용CCK-8방법측정세포활성；AnnexinⅤ-PI방법측정세포조망솔，채용Western blot기술재단백수평측정조망상관인자BCL-2、Bax화caspase-3적표체。결과수착이류화이신농도적증고，세포활성월저，세포조망솔월고；수착이류화이신작용시간적연장，세포활성월저，세포조망솔야월고。기차이균유통계학의의。Western blot결과현시：여대조조비교，이류화이신하조caspase-3단백적표체，Bax/BCL-2적비례승고병반수착Bax단렬。결론이류화이신이시간화제량의뢰적방식억제 LY8세포생장화유도조망，유도조망적궤제가능여선립체통로상관，병반수착Bax단렬。
Objective To investigate the mechanism of arsenic disulfide (As2S2) on the apoptosis of LY8 human diffuse large B cell lymphoma (DLBCL) cells. Methods LY8 cells were treated with various concentrations of As2S2 for different time periods. Cell viability was evaluated by the CCK-8 assay;Cell apoptosis was detected by AnnexinⅤ-PI analysis. The expression levels of Bax, Bcl-2 and caspase-3 were examined by western blotting. Results We found that the apoptotic rates of LY8 cells were significantly enhanced and the viability of LY8 cells was notably reduced following treatment with As2S2 for 24 h, 48 h and 72 h. Along with increasing As2S2 concentration, the apoptotic rates of LY8 cells were increased and the viability of LY8 cells was decreased. The results were both statistically significant .Western blot analysis revealed that As2S2 increased the Bax/BCL-2 protein ratio in contrast to decreased caspase-3 expression in LY8 cells. Our findings also demonstrated that Bax was proteolytically cleaved in LY8 cells. Conclusions As2S2 inhibited proliferation and induced apoptosis of LY8 cells in a time-and-dose-dependent manner. The effect was partly owing to the induction of mitochondria-dependent apoptosis involving Bax cleavage.