2014Shandong Daxue er-bi-hou-yan xuebaoRequires access

Apoptosis of Hep-2 cells induced by celecoxib

Zhao Yong-qian

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Abstract

Objective To investigate the mechanism of celecoxib,a COX-2 inhibitor,in inducing cell apoptosis in human laryngocarcinoma Hep-2 cells.Methods MTT was used to observe the proliferation of Hep-2 cells treated with various doses of celecoxib.Cell apoptosis was determined by flow cytometry and morphologic observation under fluorescent microscopy with Hoechst33258 staining.Protein expressions of Bax,Bcl-2,COX-2 were examined by western blot.Caspase-3 activation was examined by western blot.Results MTT results showed that celecoxib could inhibit the proliferation of Hep-2 cells in a time-and concentration-dependent manner.Hoechst33342 fluorescent staining showed the nucleus gradually appeared agglutination and fragmentation after the treatment of celecoxib.Apoptosis rate in the groups treated with 70 and 100 μ mol / L celecoxib were(28.9 ± 2.74) % and(32.7 ± 3.96) % correspondingly.Ww estern blot showed that celecoxib could down-regulate the levels of expressions of COX-2 and Bcl-2 protein,up-regulate Bax protein's expression,and activate caspase-3.Conclusion Celecoxib can effectively inhibit the proliferation of Hep-2 cells and induce the apoptosis of Hep-2 cells.The induction of apoptosis may be related to the increased Bax / Bcl-2 ratio and activation of caspase-3.

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Objective To investigate the mechanism of celecoxib,a COX-2 inhibitor,in inducing cell apoptosis in human laryngocarcinoma Hep-2 cells.Methods MTT was used to observe the proliferation of Hep-2 cells treated with various doses of celecoxib.Cell apoptosis was determined by flow cytometry and morphologic observation under fluorescent microscopy with Hoechst33258 staining.Protein expressions of Bax,Bcl-2,COX-2 were examined by western blot.Caspase-3 activation was examined by western blot.Results MTT results showed that celecoxib could inhibit the proliferation of Hep-2 cells in a time-and concentration-dependent manner.Hoechst33342 fluorescent staining showed the nucleus gradually appeared agglutination and fragmentation after the treatment of celecoxib.Apoptosis rate in the groups treated with 70 and 100 μ mol / L celecoxib were(28.9 ± 2.74) % and(32.7 ± 3.96) % correspondingly.Ww estern blot showed that celecoxib could down-regulate the levels of expressions of COX-2 and Bcl-2 protein,up-regulate Bax protein's expression,and activate caspase-3.Conclusion Celecoxib can effectively inhibit the proliferation of Hep-2 cells and induce the apoptosis of Hep-2 cells.The induction of apoptosis may be related to the increased Bax / Bcl-2 ratio and activation of caspase-3.

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Available abstract

Objective To investigate the mechanism of celecoxib,a COX-2 inhibitor,in inducing cell apoptosis in human laryngocarcinoma Hep-2 cells.Methods MTT was used to observe the proliferation of Hep-2 cells treated with various doses of celecoxib.Cell apoptosis was determined by flow cytometry and morphologic observation under fluorescent microscopy with Hoechst33258 staining.Protein expressions of Bax,Bcl-2,COX-2 were examined by western blot.Caspase-3 activation was examined by western blot.Results MTT results showed that celecoxib could inhibit the proliferation of Hep-2 cells in a time-and concentration-dependent manner.Hoechst33342 fluorescent staining showed the nucleus gradually appeared agglutination and fragmentation after the treatment of celecoxib.Apoptosis rate in the groups treated with 70 and 100 μ mol / L celecoxib were(28.9 ± 2.74) % and(32.7 ± 3.96) % correspondingly.Ww estern blot showed that celecoxib could down-regulate the levels of expressions of COX-2 and Bcl-2 protein,up-regulate Bax protein's expression,and activate caspase-3.Conclusion Celecoxib can effectively inhibit the proliferation of Hep-2 cells and induce the apoptosis of Hep-2 cells.The induction of apoptosis may be related to the increased Bax / Bcl-2 ratio and activation of caspase-3.

Key concepts: Celecoxib, Apoptosis, Western blot, Flow cytometry, Fragmentation (computing), Molecular biology, DNA fragmentation, Cell growth

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