内质网应激在双氢青蒿素诱导人肝癌HepG2细胞凋亡中的作用研究的中期报告摘要：本研究旨在探讨内质网应激在双氢青蒿素（DHA）诱导人肝癌HepG2细胞凋亡中的作用。实验结果表明，DHA能够显著抑制HepG2细胞的增殖，并引起细胞凋亡。此外，DHA还能够增加内质网应激标志物CHOP和GRP78的表达。通过使用五氧化二钒预处理细胞，可以明显减轻DHA引起的细胞凋亡，并减少内质网应激标志物的表达。此外，使用内质网应激抑制剂糖皮质激素可以降低DHA诱导的细胞凋亡率。以上结果表明，内质网应激在DHA诱导HepG2细胞凋亡中发挥着至关重要的作用。这项研究有助于进一步了解DHA诱导细胞凋亡的机制，并为DHA的开发提供了新的思路。关键词：内质网应激；双氢青蒿素；细胞凋亡；HepG2细胞Abstract:Theaimofthisstudywastoinvestigatetheroleofendoplasmicreticulumstressindihydroartemisinin-inducedapoptosisofhumanlivercancerHepG2cells.TheresultsshowedthatdihydroartemisinincouldsignificantlyinhibittheproliferationofHepG2cellsandinducecellapoptosis.Moreover,dihydroartemisininincreasedtheexpressionofendoplasmicreticulumstressmarkersCHOPandGRP78.Pre-treatmentofcellswithvanadylpentoxidecouldsignificantlyalleviatedihydroartemisinin-inducedcellapoptosisandreducetheexpressionofendoplasmicreticulumstressmarkers.Inaddition,treatmentwithendoplasmicreticulumstressinhibitordexamethasonecouldreducedihydroartemisinin-inducedcellapoptosis.Theseresultsindicatethatendoplasmicreticulumstressplaysacrucialroleindihydroartemisinin-inducedapoptosisofHepG2cells.Thisstudyhelpstofurtherunderstandthemechanismofdihydroartemisinin-inducedapoptosisandprovidesnewideasforthedevelopmentofdihydroartemisinin.Keywords:endoplasmicreticulumstress;dihydroartemisinin;apoptosis;HepG2cells