和厚朴酚促进肺癌细胞凋亡的分子机制研究  

Investigation on the molecular mechanism of honokiol in promoting apoptosis of lung cancer cells

作　　者：Nishimwe Ange 张凌志 孙浚皓 彭博远 杨博文 吴志浩[1,2] NISHIMWE Ange;ZHANG Lingzhi;SUN Junhao;PENG Boyuan;YANG Bowen;WU Zhihao(Research Laboratory of Tumor Microenvironment,Wannan Medical College,Wuhu 241002,Anhui,China)

机构地区：[1]皖南医学院肿瘤微环境研究室,安徽芜湖241002 [2]皖南医学院医学生物学教研室,安徽芜湖241002

出　　处：《皖南医学院学报》2024年第4期311-315,共5页Journal of Wannan Medical College

基　　金：国家自然科学基金项目(81872371);安徽省自然科学基金项目(1708085MH203);分子肿瘤学国家重点实验室开放课题(SKL-KF-2019-11)。

摘　　要：目的:研究和厚朴酚(HNK)对H1299、H460细胞凋亡的影响,并初步探讨其相关分子机制。方法:体外培养非小细胞肺癌(NSCLC)H1299、H460细胞,用不同浓度的HNK处理48 h。采用MTT法检测细胞活力;采用流式细胞术检测细胞凋亡及细胞周期抑制情况;采用Western blot检测PDZ结合基序的转录共激活因子(TAZ)、聚腺苷二磷酸核糖聚合酶(PARP)、Bcl-2、caspase-3等蛋白的表达量。结果:H1299和H460细胞经HNK处理后,与对照组相比,各浓度组细胞活力均下降且在各处理时间下细胞活力均下降(P<0.05);Western blot结果显示TAZ、Bcl-2蛋白表达量随着HNK浓度的增加而降低;cleaved-caspase3、cleaved-PARP蛋白表达量随着HNK浓度的增加而增加;caspase-3和PARP蛋白表达量随HNK浓度的增加而无明显变化;不同浓度HNK处理后,与阴性对照组相比,细胞凋亡率增加(P<0.05);HNK处理后过表达TAZ,与阴性对照组相比,细胞凋亡率降低(P<0.05)。结论:HNK可以促进NSCLC H1299和H460细胞的凋亡,其机制可能是通过抑制TAZ发挥作用。Objective:To investigate the effect of honokiol(HNK)on the apoptosis of H1299 and H460 cells,and preliminarily explore its related molecular mechanisms.Methods:Non-small cell lung cancer(NSCLC)H1299 and H460 cells were cultured in vitro and treated with different concentration of HNK for 48 hours.MTT and flow cytometry were used to respectively detect the cell viability,apoptosis and cycle inhibition.Western blot was performed to measure the protein expression levels of TAZ,PARP,Bcl-2,and caspase-3.Results:After treatment with HNK,the viability of H1299 and H460 cells was decreased in all concentration groups and at all treatment time point compared to the control group(both P<0.05).Western blot determination revealed that the expression levels of TAZ and Bcl-2 proteins were down-regulated with added HNK concentration,yet the expression levels of cleaved-caspase3 and cleaved-PARP proteins were increased with increment of HNK concentration,and the expression levels of caspase-3 and PARP proteins did not show any significant changes with addition of HNK concentration.After treatment with different concentration of HNK,the apoptosis rate amplified(P<0.05),and overexpression of TAZ resulted in decrease in cell apoptosis rate compared to the negative control group(P<0.05).Conclusion:HNK can promote apoptosis of NSCLC H1299 and H460 cells,and its mechanism may be mediated by inhibition of TAZ.

关 键 词：和厚朴酚 细胞凋亡 PDZ结合基序的转录共激活因子 非小细胞肺癌 

分 类 号：R285.5[医药卫生—中药学] R734.2[医药卫生—中医学]