Abstract:

The present work was undertaken to explore the molecular mechanisms for the apoptosis of esophageal
cancer cells induced by HPC through regulating the expression of cyclooxygenase-2 (COX-2) via the PI3K/Akt signal
pathway. Esophageal cancer cells were nurtured routinely at HPC concentrations of 25, 50, 100, 200, 300 and 400 μg/mL.
The cell counting kit-8 (CCK-8) assay was used to detect and calculate the inhibitory rate of esophageal cancer cells after
72 hours of culture. The IC50 of 250 μg/mL was chosen as the experimental group. Western blotting was adopted to detect
the degree of PI3K/Akt phosphorylation and the protein expression levels of Caspase-3 and COX-2. RT-PCR was used to
evaluate the expression level of COX-2 mRNA. Annexin V-FITC/PI was used to test inhibitory rate of esophageal cancer
cells after 0, 12, 24, 36, 48 and 72 h. The degree of PI3K and Akt phosphorylation declined gradually as the culture time
elapsed and reached the lowest point (P < 0.01) after 48 hours in the experimental group, while the opposite trend was
observed for the control group (P < 0.01) . The expression of COX-2 mRNA in the experimental group was significantly
lower (P < 0.01) compared to that in the control group. Under the action of HPC, the expression of Caspase-3 protein
was the strongest (P < 0.01) after 48 and 72 hours while the expression of COX-2 protein was the lowest (P < 0.01) after
72 hours. The apoptosis rate of esophageal cancer cells increased as the culture period was prolonged, which reached
63.54% (P < 0.01) after 72 hours of culture. HPC can exert a pro-apoptotic effect on esophageal cancer cells by reducing the
expression level of COX-2 through the PI3K/Akt signal pathway.

Key words: hawthorn procyanidins, cyclooxygenase-2, esophageal cancer, cell apoptosis