Fig. 2. CP exposure resulted in DNA damage and apoptotic cell death, which was accompanied with the activation of MAPKs, and alterations in inflammatory mediators and oxidative stress markers in HCE cells.

HCE cells were exposed to 50 μM CP for 24 h. After exposure, cell lysates were prepared and western immunoblotting for DNA damage and apoptotic cell death markers [H2A.X and p53 phosphorylation, p53 accumulation, cleaved caspase-3, and cleaved-PARP (A)], MAPKs activation [JNK1/2, ERK1/2, and p38 phosphorylation and accumulation (B)], inflammatory mediator [COX-2 (C)], and oxidative stress marker [HO-1 (D)] expression was carried out as detailed under Materials and Methods section. Protein loading was checked by stripping and re-probing the membranes for beta-actin. The results obtained were quantified by densitometric analyses of the immunoblots and fold change compared to control was calculated. C, control; CP, chloropicrin.