Paeonol increases HepG2 cells to endoplasmic reticulum stress-induced apoptosis

• 1、Department of Oncology , The First Affiliated Hospital of Anhui Medical University，Hefei 230022
• 2、Department of Oncology , The Fourth Affiliated Hospital of Anhui Medical University,Hefei 230022

Abstract：Objective To explore the effects of Paeonol on endoplasmic reticulum (ER) stress- induced apoptosis in HepG2 cells. Methods Viability and apoptosis was assessed using the MTT assay and Tunel staining to determine the effect of the ER stress inducer, tunicamycin on HepG2 cells and HL-7702. Changes in protein expression of COX-2 and GRP78 (a hallmark of ER stress) in both HepG2 and HL-7702 cells were observed through western blotting. Apoptosis was assessed using Tunel staining to determined the effect of celecoxib on ER stress-induced apoptosis. Viability and apoptosis was assessed using the MTT assay and Tunel staining to determined the effect of Paeonol on ER stress-induced apoptosis. The effect of Paeonol on ER stress-induced COX-2 was assessed using western blot analysis. Results Growth inhibition of tunicamycin on HL-7702 was dose dependent. But the growth inhibition of tunicamycin on HepG2 cells reached maximum inhibition in cells. Similar results were observed in TUNEL staining.Furthermore, the expression of cyclooxygenase-2 (COX-2) was increased in HepG2 cells but not in HL-7702 cells. Down-regulation of COX-2 expression using the COX-2 inhibitor, celecoxib, increased tunicamycin-induced apoptosis.However, co-treatment with tunicamycin and Paeonol significantly increased the rate of apoptosis .Co-treatment with tunicamycin and Paeonol also decreased the expression of COX-2.Conclusion:Paeonol increases HepG2 cells to ER stress-induced apoptosis by down-regulating COX-2 expression.

Keywords： hepatocellular carcinoma endoplasmic reticulum stress apoptosis Paeonol