Cyanidin-3-glucoside Intervents UVB-induced ROS/COX-2 Pathway In HaCaT Cells

Objective:To investigate the mechanism of Cyanidin-3-glucoside (C3G) intervents UVB-induced ROS/COX-2 pathway in HaCaT cells.Methods1. The dose of UVB induced oxidative damage in HaCaT cells were elected by MTT assay and fluorescence measurement.2. The effect of C3G on morphology in UVB-induced HaCaT cells was observed by microscope.3. The cell viability of C3G in UVB-induced HaCaT cells was tested by MTT assay.4. The effect of C3G on ROS in UVB-induced HaCaT cells was detected by fluorescence measurement.5. Western blot was used to analys the effects of C3G on the expressions of COX-2, p-EGFR, p-ERK, p-p38, p-JNK and p-Akt in UVB-induced HaCaT cells.Results:1. An oxidative damage model was established by 300 mJ/cm2 UVB irradiated HaCaT cells.2. C3G (80～200 mol/L) reduces the damage of cell morphology in UVB-induced HaCaT cells.3. It was found that the cell viability of C3G group (80～200 mol/L) increase compared with UVB controls after cells following UVB irradition were incubated for 12 hour (P< 0.05).4. The quantity of ROS were decreased significantly in C3G group (80～200 mol/L) after UVB irradiation (P< 0.05).5. C3G (80～200 mol/L) and celecoxib (80mol/L) could decrease the expression of COX-2 and disturb the activities of EGFR, ERK, p38, JNK and Akt in the oxidative damage model.Conclusion:1. UVB caused HaCaT cells oxidative damage.2. UVB irradiated HaCaT cells could increased ROS generation, which induced activation of EFGR, increased the phosphorylation of ERK, p38, JNK and Akt, and enhancing the expression of COX-2. It is the UVB-induced ROS/COX-2 pathway in HaCaT cells.3. C3G could reduce the level of ROS and protect the cell viability of UVB irradiated HaCaT cells.4. C3G suppresses UVB-induced ROS/COX-2 pathway in HaCaT cells by inhibiting ROS generation, which reduc the expression of COX-2.