Dihydromyricetin promotes apoptosis,suppresses proliferation and tumor necrosis factor-α-mediated nuclear factor kappa-B activation in nasopharyngeal carcinoma CNE-2 cells

• 作者: LI Caihong SHI Jinlian HUANG Bo DING Hang LIN Hanguang ZENG Jincheng ZHAO Yang LUO Guoqing
• 来源期刊: 中医杂志（英文版）
• 年，卷（期）: 2021,（3）
• 所属期刊栏目: Research Articles
• 页码范围: 367-375
• 页数: 9页
• 语种: 英文
• DOI: 10.19852/j.cnki.jtcm.2021.03.004

摘要

OBJECTIVE:To investigate the efficacy of dihydro-myricetin(DMY)on nasopharyngeal carcinoma(NPC)cell proliferation,apoptosis and to reveal the underlying mechanism in vitro experiments.METHODS:The CNE-2 cell line was treated with dif-ferent concentrations of DMY and the effects of DMY on cell viability and proliferation were evaluat-ed using cell counting kit-8(CCK-8)assay and plate colony formation assay.Cellular apoptosis was de-tected by flow cytometry following Annexin V fluo-rescein isothiocyanate/propidine iodide staining.Nuclei morphology was observed under a fluores-cence microscope following Hoechst 333258 stain-ing.The expression of phosphorylated inhibitor of nuclear factor kappa-B kinase subunit beta(p-IKKβ),phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha(p-IKKα),inhibitor of nuclear factor kappa-B alpha(IκB-α),nuclear factor kappa-B(NF-κB)/p65 was examined by Western blot analysis and the nuclear translocation of NF-KB/p65 was observed using a confocal laser scanning microscopy.RESULTS:DMY inhibited the proliferative capabili-ty and colony formation of NPC CNE-2 cells.Mean-while,DMY induced apoptosis of CNE-2 cells in a dose and time-dependent manner via upregulat-ing B-cell lymphoma-2 associated X,but downregu-lating B-cell lymphoma-2 and pro-caspase-3.Im-portantly,we found that DMY suppressed tumor necrosis factor alpha(TNF-α)-mediated NF-κB acti-vation via inhibiting p-IKKβ,p-IKKα and blocking NF-κB subunit p65.CONCLUSION:Our experiments demonstrated that DMY had significant antiproliferative and apoptosisinducing effects on CNE-2 cells.Addition-ally,DMY promoted inactivation of p-IKKβ,p-IKKα,and blocked the nuclear translocation of NF-κB sub-unit p65.These results suggest that DMY may be an important therapeutic approach for NPC.