Research On Impact Of Proliferation And Apoptosis Of Parthenolide And Combined With Adriamycin And Dexamethasone To Jurkat Cells

Objective:To explore the effects of cytotoxicity and the apoptosis ofparthenolide (PTL) to Jurkat cells and its mechanisms,and to explore the effectsof cytotoxicity and the apoptosis of parthenolide (PTL) combined withadriamycin and dexamethasone to Jurkat cells and the mechanisms，PTL isprovided as experimental basis for the clinical application of anti-leukemia.Method：Using The Jurkat cells of lymphocyte leukemia as the research object,we calculate half inhibitory concentration (IC50) of PTL (40,20,15,10,5,2.5,1u mol/L) for24h,48h,72h,and IC50of DEX (10,20,50,100,250,500,250umol/L), ADR (0.25,0.5,0,75,1,2,4,8u mol/L) after48h。MTT method wasused to detect proliferation inhibition effects of the PTL combined respectivelywith DEX, ADR to JUIRKAT cells for48hours; Using flow cytometry detectiontest morphological changes and apoptosis rates of PT Land PTL combinedrespectively with DEX, ADR on JUIRKAT cells for48hours; Usingimmunohistochemical method to detect the expression of protein NF-κBp65ofPTL and PTL combined respectively with DEX, ADR on JUIRKAT cells for48 hours.Results:5-20u mol/L PTL can significantly inhibit cell proliferation,inhibition of cell proliferation with the increase of concentration of PTL andfunction extended and enhanced gradually(r=0.837,P＜0.01). IC50of PTL for24,48,72h of were4.71±1.32,8.11±1.96and1.96±1.54u mol/L（F=87.56,P均<0.01. IC50of ADR and DEX concentration dependence to inhibit Jurkat cellsproliferation for48h were0.53,324.35u mol/L（r=0.956，r=0.853，P＜0.01）.0,5,10u mol/L PTL processing, Jurkat cells apoptosis rates after48h were4.2±1.23%,10.5±2.03%and22.1±2.28%,(F=68.32，p <0.01),and the NF-κB/p65positive integral were statistical different (F=78.25，p<0.01). Inhibition rates of2,4,8,16u mol/LPTL combined with500u mol/L DEX, and0.25u mol/L ADR onJurkat cells for48h increased significantly ((F=123.86，p<0.05). Using DEX,ADR, PTL and PTL combined with DEX and ADR on Jurkat cells,apoptosisrates of the48h were (64.13±4.62)%,(68.18±4.11)%,(25.18±3.07)%,(77.05±4.35)%,(81.68±4.56)%, the apoptosis rates of the experimental groupswere higher than the control group (5.25±1.4)%(F=107.32，p<0.01), apoptosisrates of PTL combined with DEX and ADR groups were obviously higher thanDEX and ADR groups (F=116.25，p<0.01). Among the NF-κBp65of Single PTL,PTL combined with DEX and ADR after48h on Jurkat cells,the NF-κBp65ofDEX positive score were significantly lower than the control group (F=106.55，p<0.01), while ADR single group was significantly higher than the control group(F=,73.28，p=0.00), PTL jointing groups were significantly lower than that of alone group (F=56.52，p<0.01).Conclusion: PTL has the effect of inhibitingproliferation and apoptosis to Jurkat cells, and can inhibit the NF-κBp65signalpathway, and strengthen ADR, DEX Jurkat leukemia cells proliferation inhibition,and promote the apoptosis.