Figure 10.

Juglanin functions as the inhibitors of MAPKs and NF-κB (p65) to attenuate UVB-induced skin injury in vitro. HaCaT cells were pre-treated with (A) SB203580 (50 nM), (B) PD98059 (10 nM) and (C) SP600125 (50 µM) for 1 h or/and with juglanin exposure for 12 h, and then exposed to 15 mJ/cm² of UVB irradiation for 24 h, followed by incubation for another 12 h in the absence or presence of juglanin. Phosphorylated p38, ERK1/2 and JNK were calculated using western blot analysis. (D) The cells were pre-treated with NF-κB (p65) inhibitor, JSH-23 (8 µM), for 1 h or/and with juglanin exposure for 12 h, and then exposed to 15 mJ/cm² of UVB irradiation for 24 h, followed by incubation for another 12 h in the absence or presence of juglanin (160 µM). Phosphorylated p38 was calculated using western blot analysis. ERK1/2 activation was measured using western blot analysis. (E) The cells after treatment as indicated were harvested for RT-qPCR analysis of COX2, IL-1β and TNF-α. Data are represented as the mean ± SEM, n=8. ^*P<0.05, and ^***P<0.001. p, phosphorylated; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinases; NF-κB, nuclear factor-κB; UVB, ultraviolet B.