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Effect Of Pravastatin On Apoptosis In Human Lung Adenocarcinoma Cell Line A549

Posted on:2017-02-05Degree:MasterType:Thesis
Country:ChinaCandidate:F H YangFull Text:PDF
GTID:2334330485993013Subject:Internal Medicine
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BackgroundMalignant tumor(malignant tumor,MT)is a disease characterized by abnormal cell differentiation,proliferation,and loss of cell growth control.In recent years all over the world,MT cases related with environment pollution and unhealthy lifestyle has been growing incresingly,and lung cancer has become the first of MT death causes in China,accounting for 22.7% of all.In addition,study of cancer epidemiology finds that with the popularity of smoking since the 1920 s,the incidence and mortality of lung cancer has begun to rise and will continue in the future.Currently,the most common clinical type of lung cancer is non-small cell lung cancer(non-small cell lung cancer,NLCSC),which accounts for 80% of all lung cancers.From the end of the 20-century,the incidence of Lung adenocarcinoma,(AC),one kind of NLCSC lung cancer,has been increasing,and it has replaced squamous cell lung carcinoma(SCC)to become the most common lung cancer pathologic type.AC,because of its long incubation period,it cannot be diagnosed until it develops to be an advanced cancer,and in recent years with the gradually increasing pressure of life,the incidence of end-stage AC appears obviously as a trend,which attracts the attention of the whole academic world.Therefore,looking for a safe and effective drug to treat advanced AC is of great clinical significance.ObjectiveThis experimental study aims at preliminary exploration and analysis of effect of pravastatin(pravastatin,prav)on apoptosis of human lung adenocarcinoma A549 cells and effect of prav of Bax and Bcl-2 in A549 cell apoptosis,to explore the possible anti-tumor mechanism,explore the optimal drug concentration,and offer a solid theoretical basis forstatins in lung cancer prevention and treatment of clinical application.Methods1.First,cultivate human lung adenocarcinoma cells A549 in vitro according to the conventional way.Then observe the influence of prav groups with different concentrations(0 umol / L,20 umol / L,40 umol / L,80 umol / L,160umol/L)and different time groups(24 h,48 h,72 h)on cell proliferation using methyl thiazolyl tetrazolium(incubated a colorimetric assay and MTT method),so as to select the appropriate concentration of drug and appropriate action time.Thirdly,according to the results of MTT,set control group and the experimental group(0 umol/L,40 umol/L,80 umol/L,160 umol/L).2.Detect the apoptotic rate of A549 cells in each group by flow cytometry(flow cytometry,FCM).3.Detect the rate of protein expression of Bax and Bcl-2 in A549 cells by blot Western method.Results1.MTT results showes that different concentrations of pravastatin on human lung adenocarcinoma cell line A549 24 h,48h,72 h after the cell proliferation inhibition rates are significantly enhanced(P < 0.05),different concentration compared with the control group at the same time,the inhibition is significantly enhanced(P < 0.05),also increased at the same concentration of 24 h compared with the inhibition(P < 0.05);inhibition of PRAV on proliferation of human lung adenocarcinoma A549 cells,the inhibition showes dose effect relationship between concentration and time(P < 0.05).2.Flow cytometry assay showes 40,80,160?mol / L pravastatin group apoptosis rates of the cells after 48 h respectively are significantly increased(P <0.05);with the increase of drug concentration PRAV,apoptosis rate of A549 cells gradually increases,and shows a dose-dependent manner(P<0.05).3.Western blot results shows that with the increase of PRAV concentration,theexpression of Bax A549 cells increases,while the expression of Bcl-2 gradually reduces.ConclusionsPRAV has an inhibitory effect on proliferation of human lung adenocarcinoma A549 cells.Its mechanism may be related to the increasing Bax apoptosis gene expression,while the expression of Bcl-2 gradually reduces.
Keywords/Search Tags:lung adenocarcinoma A549 cells, PRAV, apoptosis, Bax, Bcl-2
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