ABSTRACT
Objective To investigate the effect of quercetin on suppressing the proliferation,migration and invasion of A549 cells via the signal transducer and activator of transcription 3(STAT3)signaling pathway. Methods The A549 cells were cultured in vitro and treated with quercetin at various concentrations(0,7.5,15,30,60 and 120μmol/L)for 24 h,48 h and 72 h. The proliferation of A549 and the 50%inhibitory concentration(IC50)were measured by the cell counting kit-8(CCK-8). The A549 cells treated for 24 h were randomly divided into 4 groups:the blank control,15 and 30 μmol/L quercetin,and 3 μg/ml cisplatin(the positive control) groups. The effect of quercetin on adhesion rate was detected by the cell adhesion assay;the cell migration ability was evaluated by the wound healing assay;the cell invasion ability was evaluated by the Transwell chamber assay;the expression of STAT3 and phosphory?lated-STAT3(p-STAT3)proteins were detected by Western blot assay. Results Quercetin inhibited A549 cell growth dose-depend?ently. Compared with the blank control group,quercetin could significantly inhibit the adhesion rate,migration ability and invasion of A549 cells(P<0.05 or P<0.01);compared with the blank control group,quercetin significantly inhibited STAT3 and p-STAT3 ex?pression level(P<0.05 or P<0.01). Conclusion Quercetin could inhibit the proliferation,migration and invasion of A549 cells, and the mechanism is libely related to the STAT3 signal pathway.
ABSTRACT
Objective To observe the effects of capsaicin on PGE2 concentration of IL-1β-induced human large cell carcinoma NCI-H460 cells,and further observe its effect on COX-2 and mPGES-1 so as to explore the possible mechanisms against non-small cell lung cancer.Methods NCI-H460 cells were cultured in vitro ;the effect of capsaicin in inhibiting NCI-H460 cells proliferation was observed.The 50% inhibitory concentration (IC50 ) was measured by MTT assay.IL-1βstimulation method was used to construct inflammation model,and the effects of capsaicin on COX-2 activity and PGE2 concentration in NCI-H460 cells were measured by ELISA.The effects of capsaicin on COX-2 and mPGES-1 protein level in NCI-H460 cells were analyzed by Western blot;the effects of capsaicin on COX-2 mRNA and mPGES-1 mRNA expressions in NCI-H460 cells were analyzed by Real-time PCR. Results MTT assay results showed that the growth of NCI-H460 cells treated with capsaicin was significantly inhibited compared with the control group (P <0.05 or P <0.01 ).Capsaicin could significantly decrease COX-2 activity and PGE2 concentration in NCI-H460 cells,and significantly decrease COX-2,mPGES-1 protein levels as well as COX-2,mPGES-1 mRNA expressions in NCI-H460 cells in a dose-dependent manner compared with the control group (P < 0.05 ).Conclusion Capsaicin inhibits the release of PGE2 by downregulating COX-2 and mPGES-1 mRNA expressions in NCI-H460 cells,which may be one mechanism of its effect against non-small cell lung cancer.
ABSTRACT
Objective To investigate the expression of p38 MAPK gene and p38 MAPK protein,and explore the effect of p38 MAPK in inflammation reaction of severe acute pancreatitis.Methods 48 cases with severe acute pancreatitis were chosen as research group,and another 48 healthy cases as control group.The expression of p38 MAPK gene were investigated by RT-PCR,and the expression of p38 MAPK and P-p38 MAPK protein were investigated by western blot. Results The expression of p38 MAPK mRNA,p38 MAPK protein and P-p38 MAPK protein in research group were higher than that in control group,the differences were all statistically significant(P<0.05 ).Conclusion The expression of p38 MAPK gene and p38 MAPK protein were significantly increased in patients with severe acute pancreatitis,which showed that p38 MAPK played an important role in inflammation reaction.