The Effect And Molecular Mechanism Of Celecoxib In U251 Glioma Cell Proliferation And Apoptosis

Objective:To investigate the effect of celecoxib in human malign glioma U251 cell proliferation and the distribution of the expression of nuclear factors(NF-κB) affected by celecoxib in cells。Methods:Human Glioma line (U251) were incubated with different concentrations of Celecoxib(0,10,25,50,100 umol/l respectively) or with TNF-α(50 ng/ml),respectively.The proliferation rates of the U251 were determined by MTT assay. The expression in the intracellular and nucleus of NF-κB(p65) was measured after treatment with Celecoxib by immunohistochemistry and western blotting。To observe the location of NF-κB(p65) after TNF-αwith celecoxib stimulation by immunohistochemistry,to investigate the nucleus of NF-κB(p65) protein level by means of Western blot technique.Results:MTT assay indicated that the proliferation rates of U251 induced with different concentrations of Celecoxib were significantly reduced in a does-dependent manner,The combination with TNF-α(50 ng/ml) has no synergy(P>0.05)。IHC:The protein of NF-κB(p65) of the U251 are being both in the cytoplasm and the nucleus at quiescent condition.after TNF-αstimulation,NF-κB(p65) translocation into the nucleus obviously at 30 minutes.U251 were pre-treated with Celecoxib for 1h and then with TNF-α.Celecoxib prevents TNF-α-induced NF-κB(p65) translocation into the nucleus. In addition, the nucleus of NF-κB(p65) protein level was induced by Celecoxib in a dose-dependent manner, and it was lower than those without treatment.Conclusion:1. Celecoxib inhibits cell growth and induces apoptosis in U251 cell in a dose-dependent manner.2. Celecoxib can effectively inhibit TNF-α-induced NF-κB(p65) translocation into the nucleus.3. Celecoxib inhibits cell proliferation in U251 cell ,which may be mediated by inhibiting nuclear translocation.