Explore Lumiracoxib may induce cancer cell apoptosis mechanism. Methods: The human lung cancer cell line A549 and NCI H460 cells were added to a final concentration of IL-1β1 1 μg / L stimulated 24 h, then added different concentrations Lumiracoxib cultured 24 h, using the Western blot assay ERK2, p-ERK and Bcl-2 expression levels. Lumiracoxib vitro processing A549, NCI-H460, the use by Western blot Bcl-2, Bax expression levels. Results: Lumiracoxib role in lung cancer cells after ERK2 and p-ERK phosphorylation levels were decreased, accompanied by decreased levels of Bcl-2, the difference was statistically significant (P <0.01). And with Lumiracoxib concentration increased, Bcl-2 protein expression was decreased, while Bax protein expression in A549 cells enhanced in NCI-H460 cells unchanged, Bcl-2/Bax ratio decreased. Conclusion: Lumiracoxib induce apoptosis in lung cancer cells may be related through the ERK signal transduction pathway in lung cancer cells to produce Bcl-2, thereby inducing Bcl-2/Bax ratio decline.
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