Celecoxib enhances apoptosis of the liver cancer cells via regulating ERK/JNK/P38 pathway.

Purpose We aimed to investigate the effect of celecoxib on rats with liver cancer through the extracellular signal-regulated kinase (ERK)/c-Jun N-terminal kinase (JNK)/p38 pathway. Methods Sprague-Dawley rats (n=36) were divided into 3 groups (n=12 per group) randomly. In model group, the liver cancer model was established, and normal saline was intraperitoneally injected. In celecoxib group, the liver cancer model was also established, and celecoxib was intraperitoneally injected. After intervention for 30 d, the samples were taken. The body weight of rats was measured before modeling and before sampling. The morphology of liver tissues was observed via hematoxylin-eosin (HE) staining, the expressions of related proteins and messenger ribonucleic acids (mRNAs) were determined via Western blotting and quantitative polymerase chain reaction (qPCR), respectively, and the protein expressions of cysteinyl aspartate specific proteinase 3 (Caspase3) and Cyclin D1 in liver tissues were detected. Results Before modeling, there was no difference in t.