gper抑制px对雌激素作用下子宫内膜癌细胞增殖、凋亡的影响.pdfVIP

X4．AnnexinII1717 III AbstractAKTAAMethodsmechanismAbstract-mediatedBcl-2HEC-1HEC-1AHEC-1HEC．1ASOEndometrialGGPERGPERGPERGPERhaveGPERGPER-inducedGGPER-inducedaahasntnewreducesrelatedresearchoneonouroccurrenceonEffectGoncancercancancauseandandandandafteractivatedandandofofofofofofoxidativeofofofofofobserveofofoutsideetctoetetofemalefoundfoundandandandandandandandandandandchanceclassiccalledcellscellcellscarcinomacellcellsconsistentcellcellcellsdiscusscellsofandfar．Thisthethreetumorstheendometrialeffects’’andeffects．GthatthatendometrialthatendometrialthatthetheendometrialthatthetheeffecteffectendometrialtheISthecellscancer．Thecancercancer．Previouscancercancer．IIstimulationstress—inducedstudiesstudiesshowncellslshikawa713·-estradiol--inducedIshikawaIshikawaIshkawalevelslackincreaseinclusesininducesisisisinduceinhibitorin11ininhibitorin1 Abstract HEC一1A Ishkawaand cells MTTmethod． growth 2．Determining by cancercell endometrial wimFlow instrument． 3．Determining cycle cytometry 4．TheAnnexin flow V-FITC todetectcell cytometry apoptosis． Results MTT on resultsDetermined haseffect experiment by method：E2 promoting ofIshikawacells thetime proliferation showing andtheconcentration theroleinHEC dependence①=128．954，P0．001)，while -1Acell Wasnot thereWasno proliferationsignificant(F=0．955，P=0．393)，and statistical thedifferencesthe significance(F=1．978，P=0．137)betweenamong concentration．Undertheacti