Fig 2: The immunohistochemical staining of the fundic glands with NF-?B (× 200) and caspase-3 (× 200) stains. In control and MOLE groups the figure shows very weak cytoplasmic immunoreactivity for NF-?B in the cell lining of gastric glands. In BPA group there is a STRONG cytoplasmic immunoreactivity while in MOLE co-treated group the figure shows moderate cytoplasmic immunoreactivity but in MOLE pretreated group it shows WEAK cytoplasmic immunoreactivity for NF-?B in the cell lining gastric glands. The figure also shows caspase-3 staining of a longitudinal section, the fundic glands of the stomach; in control and MOLE groups, it shows weak cytoplasmic immunoreactivity in the cell lining of gastric glands. In BPA group there is a STRONG cytoplasmic immunoreactivity; in MOLE co-treated group it appears with moderate cytoplasmic immunoreactivity but in MOLE pre-treated group it shows weak cytoplasmic immunoreactivity for caspase-3 in the cell lining of gastric glands. Panels A and B illustrate the same findings. Data are expressed as mean ± SEM (n = 8). *Significant vs control group, #significant vs BPA group, $significant vs MOLE co-treated group

Fig 3: Schematic diagram of BMP-mediated activation of Puma-dependent apoptotic signaling in the pathogenesis of IDD. The decreased levels of BMPs failed to activate the BMPR1 and BMPR2 receptors on the membrane, causing the decrease of phosphorylation of Smad1/5/8 and the failed assembly of the pSmad1/5/8-Smad4 complex. The failed translocation of the pSmad1/5/8-Smad4 complex from the cytoplasm to the nucleus limits its control in the transcription of PUMA, resulting in the upregulation of PUMA. Puma induces the release of cytochrome c from the mitochondria. Cytochrome c binds to Apaf-1, which recruits caspase-9 to assemble the apoptosome, leading to the activation of Caspase-9 and Caspase-3. The activation of apoptosis causes the occurrence of IDD.