Camphorquinone (CQ) is a popularly-used
photosensitizer in
composite resin restoration. In this study, the effects of CQ on cytotoxicity and
inflammation-related genes and
proteins expression of pulp cells were investigated. The role of
reactive oxygen species (ROS), ATM/Chk2/p53 and hemeoxygenase-1 (HO-1) and
MEK/ERK signaling was also evaluated. We found that ROS and
free radicals may play important role in CQ toxicity. CQ (1 and 2 mM) decreased the viability of pulp cells to about 70% and 50% of control, respectively. CQ also induced G2/M cell cycle arrest and apoptosis of pulp cells. The expression of
type I collagen, cdc2,
cyclin B, and cdc25C was inhibited, while p21, HO-1 and
cyclooxygenase-2 (COX-2) were stimulated by CQ. CQ also activated ATM, Chk2, and p53 phosphorylation and GADD45α expression. Besides, exposure to CQ increased cellular ROS level and
8-isoprostane production. CQ also stimulated COX-2 expression and
PGE2 production of pulp cells. The reduction of cell viability caused by CQ can be attenuated by
N-acetyl-L-cysteine (NAC),
catalase and
superoxide dismutase (SOD), but can be promoted by
Zinc protoporphyin (ZnPP). CQ stimulated ERK1/2 phosphorylation, and
U0126 prevented the CQ-induced COX-2 expression and
prostaglandin E2 (
PGE2) production. These results indicate that CQ may cause cytotoxicity, cell cycle arrest, apoptosis, and
PGE2 production of pulp cells. These events could be due to stimulation of ROS and
8-isoprostane production, ATM/Chk2/p53 signaling, HO-1, COX-2 and p21 expression, as well as the inhibition of cdc2, cdc25C and
cyclin B1. These results are important for understanding the role of ROS in pathogenesis of
pulp necrosis and pulpal
inflammation after clinical
composite resin filling.