Effect Of Arsenic Trioxide Combined With Cisplatin On Lung Adenocarcinoma A549Cells Proliferation Inhibition And Fas Receptor Effects

ojective: According to the different concentrations of arsenic trioxide,cisplatin and two drug combination on the human lung adenocarcinoma A549cell growth,proliferation, cell cycle, apoptosis and expression of Fas receptor the effect of cisplatin,arsenic trioxide, and the combination of the two drugs in lung cancer cells in vitrochemotherapy effect and the possible mechanism, so as to the clinical finding newchemotherapeutic medicine and possible chemotherapeutic sensitizer to providetheoretical and experimental basis, to further improve the lung cancer chemotherapyeffect and reduce the side-effects of chemotherapy.Methods: Through in vitro culture of human lung adenocarcinoma A549cells, andin the logarithmic growth phase of the cell experiment. According to the experimentalgroup treated cells, through the MTT method for the detection of different groups ofdrugs on cell proliferation inhibition, were observed under inverted microscope drugs oncell morphology; flow cytometry in cell apoptosis and cell cycle arrest, finally byImmunohistochemistry Assay for detection of drugs on human lung adenocarcinomaA549cells in Fas receptor expression the effect of.Result:1. Arsenic trioxide, cisplatin alone drugs on human lung adenocarcinomaA549cells proliferation.Arsenic trioxide and cisplatin alone on the human lung adenocarcinoma A549cells,can inhibit cell proliferation, along with the prolongation of time and the increase of theconcentration, its effect on cell proliferation inhibition increases gradually, which is time dependent and concentration dependent characteristics.2. Different concentrations of arsenic trioxide and cisplatin on human lungadenocarcinoma A549cells morphology effect.From the morphological observation, whether arsenic trioxide or cisplatin, insmaller doses (1,2μmol/L) on human lung adenocarcinoma A549cells, cell death byapoptosis mainly exists in the form of performance for the cell shape, round, adherent ispoorer, larger doses (8μmol/L) the majority of cells showed necrosis, morphologicalchanges, under the microscope can see a large number of necrotic cellular debris.3. Effect of arsenic trioxide combined with medication on human lungadenocarcinoma A549cells proliferation.2μmol/L to cisplatin,2,4and1,8μmol/L of arsenic trioxide combined withmedication, combination therapy on human lung adenocarcinoma A549cell proliferationinhibitory effect was stronger in the group with medication alone (p<0.01), combinedwith medication, with arsenic trioxide concentration increased, and its inhibitiongradually (p <0.05), but1μmol/L of arsenic trioxide combined with cisplatin and2μmol/L combined with arsenic trioxide in cisplatin group in24hours and its inhibition ratehad no significant difference (p>0.05), along with the prolongation of time, theinhibitory effect is obviously enhanced.4. Arsenic trioxide, cisplatin and combined medication on apoptosis and cell cycleeffects.Compared with the control group,2μmol/L of arsenic trioxide and cisplatin onhuman lung adenocarcinoma A549cells48hours are inducing apoptosis (p <0.01). Thecisplatin group the apoptosis rate of arsenic trioxide apoptosis rate and greater group (p<0.05). The combination group ability to induce apoptosis far greater than medicationalone group (p<0.01,p<0.01);2μmol/L effect of arsenic trioxide human lungadenocarcinoma A549cells after48h, the performance of the G2/M its block; thecisplatin group showed S phase arrest; combined treatment group, G0/G1, the G2/Mphase were shown to cycle phenomenon. 5. Arsenic trioxide, cisplatin and combined medication on intracellular Fas receptorexpression in human lung adenocarcinoma A549cells.Experiments show that arsenic trioxide and cisplatin with upregulation of Fasreceptor expression, compared with the control group, the difference was statisticallysignificant (p<0.01). Arsenic trioxide and cisplatin group compare difference not tohave statistical significance (p>0.05). The combination group Fas receptor expression isgreater than medication alone group (p <0.01, p<0.01).Conclusion: Arsenic trioxide and cisplatin with inhibition of human lungadenocarcinoma A549cells proliferation and apoptosis effect, in effect appears on thelimitation and dose-effect relationship. Effect of arsenic trioxide on the cell cycle arrestand G2/M, cisplatin to cell cycle arrest and S. The induction of apoptosis mechanismmay be through the up-regulation of intracellular Fas receptor and the realization of.