灰树花β多糖通过激活氧化应激诱导肺癌细胞凋亡

β-glucan from maitake induces lung carcinoma cells apoptosis via activating oxidative stress

目的:研究灰树花β多糖诱导肺癌细胞凋亡的作用及机制。方法:采用CCK-8和流式细胞术检测灰树花β多糖对肺癌细胞生存活性和凋亡的影响;采用MitoSOX和TMRM染料检测线粒体ROS生成和线粒体膜电位;采用免疫印迹方法检测凋亡相关分子在细胞内的表达水平及分布。结果:灰树花β多糖能够显著抑制肺癌细胞生存活性,促进肺癌细胞凋亡;其机制可能是通过诱导肺癌细胞线粒体ROS生成增多,导致线粒体膜电位降低,促进细胞色素c释放和Bcl-2家族分子发生转位,最终导致细胞凋亡。结论:灰树花β多糖通过激活氧化应激诱导肺癌细胞凋亡。

Objective:To study the functional roles and the underlying mechanism of β-glucan from maitake on the apoptosis of lung carcinoma cells. Methods:CCK-8 and flow cytometry were used to detect the effects of β-glucan from maitake on the viability and apoptosis of lung carcinoma cells.MitoSOX and TMRM were used to determine the production of ROS and mitochondrial membrane potential,respectively.The expression and distribution of the apoptosis related molecules were measured by Western blot. Results:β- glucan from maitake significantly inhibited the growth,and promoted the apoptosis of lung carcinoma cells.Furthermore,β-glucan from maitake increased the production of ROS,followed by decreasing the mitochondrial membrane potential,promoting the releasing of Cytochrome-C and the translocating of Bcl-2 family members,which finally led to cell apoptosis. Conclusion:β-glucan from maitake induces lung carcinoma cells apoptosis via activating oxidative stress.