异黄腐酚抑制顺铂诱导的肺癌A549细胞凋亡和迁移的机制  

Mechanism of Isoxanthohumol Inhibiting Cisplatin-Induced Apoptosis and Migration of Lung Cancer A549 Cells

作　　者：王晓慧 毋乃朴 臧丹 薛云 陈亦扬 崔园园 狄文玉[1] WANG Xiaohui;WU Naipu;ZANG Dan;XUE Yun;CHEN Yiyang;CUI Yuanyuan;DI Wenyu(Pathology Department,the First Affiliated Hospital of Xinxiang Medical College,Xinxiang 453000,China;Department of General Surgery,Sanquan College of Xinxiang Medical University,Xinxiang 453000,China)

机构地区：[1]新乡医学院第一附属医院病理科,河南新乡453000 [2]新乡医学院三全学院外总教研室,河南新乡453000

出　　处：《河南医学研究》2025年第8期1375-1379,共5页Henan Medical Research

基　　金：河南省医学科技攻关计划联合共建项目(LHGJ20200504)。

摘　　要：目的 探究异黄腐酚(IN)抑制顺铂(DDP)诱导的肺癌A549细胞增殖抑制、凋亡和迁移的机制。方法 体外培养人肺癌A549细胞,随机分为Control组、DDP组和DDP+IN组。Control组A549细胞未经任何处理,DDP组A549细胞经6 mg·L^(-1)的DDP处理48 h,DDP+IN组A549细胞经6 mg·L^(-1)的DDP和10μmol·L^(-1) IN处理48 h,通过CCK-8法检测A549细胞活性,通过流式细胞仪检测A549细胞凋亡,通过transwell小室检测A549细胞侵袭和迁移能力,通过免疫印迹法检测蛋白表达。结果 与Control组相比,DDP组和DDP+IN组A549细胞活性降低、侵袭和迁移细胞数目减少(P<0.05),且DDP+IN组细胞活性高于DDP组、侵袭和迁移细胞数目多于DDP组(P<0.05)。与Control组相比,DDP组和DDP+IN组A549细胞凋亡率增加(P<0.05),且DDP+IN组细胞凋亡率高于DDP组(P<0.05)。DDP+IN组A549细胞中Bcl2关联X蛋白(Bax)、Bax/B细胞淋巴瘤/白血病-2蛋白(Bcl2)、Caspase-3和E-cadherin蛋白表达水平高于DDP组(P<0.05),而DDP+IN组A549细胞中Bcl2、Vimentin、N-cadherin和Snail蛋白表达水平高于DDP组(P<0.05)。结论 IN能够增加DDP诱导的A549细胞凋亡和侵袭/迁移抑制,其机制与IN调控凋亡相关蛋白和上皮间质转化相关蛋白的表达有关。Objective To explore the mechanism by which isohumol(IN)inhibits cisplatin(DDP)-induced proliferation inhibition,apoptosis,and migration of lung cancer A549 cells.Methods Human lung cancer cell line A549 was cultured in vitro and randomly divided into control group,DDP group,and DDP+IN group.The control group A549 cells were untreated,the DDP group A549 cells were treated with 6 mg·L^(-1) DDP for 48 hours,and the DDP+IN group A549 cells were treated with 6 mg·L^(-1) DDP and 10μmol·L^(-1) IN for 48 hours.A549 cell activity was detected by CCK-8 method,cell apoptosis was detected by flow cytometry,cell invasion and migration ability was detected by transwell chamber,and protein expression was detected by Western blotting.Results Compared with the control group,the DDP group and DDP+IN group showed a decrease in cell viability,invasion,and migration of A549 cells(P<0.05),and the DDP+IN group had higher cell viability and more invasion and migration cells than the DDP group(P<0.05).Compared with the control group,the apoptosis rate of A549 cells increased in the DDP group and DDP+IN group(P<0.05),and the apoptosis rate of A549 cells in the DDP+IN group was higher than that in the DDP group(P<0.05).Bcl 2-associated X protein(Bax),Bax/B cell lymphoma/leukemia-2 protein(Bcl 2),and Caspase-3 and E-cadherin were higher in A549 cells of the DDP+IN group(P<0.05),while Bcl 2,Vimentin,N-cadherin,and Snail were significantly higher in A549 cells than in the DDP group(P<0.05).Conclusion IN can increase DDP induced apoptosis and invasion/migration inhibition in A549 cells,and its mechanism is related to IN regulating the expression of apoptosis related proteins and epithelial mesenchymal transition related proteins.

关 键 词：肺癌 异黄腐酚 顺铂 凋亡 迁移 

分 类 号：R734.2[医药卫生—肿瘤]