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Possible molecular targets of the preventive effects of PT in Cr(VI)-induced ACD. Cr(VI) activated NLRP3 inflammasome activity and the p38 MAPK/MK2 signaling pathway leading to pro-inflammatory gene expression and resulting in keratinocyte cell death by apoptosis. The administration of PT inhibited cell death, the NLRP3 inflammasome and pro-inflammatory cytokines, which were regulated by ROS generation and ER stress and were related to Cr(VI)-induced ACD.
