Fig. 14

Molecular mechanisms of betaine on Nrf-2-Keap1 pathway and Caspase-3 activation. A: BET can inhibit the interaction between Nrf-2 and Keap1, thus enhancing the stabilisation of Nrf-2, which can translocate into the nucleus and bind to antioxidant-responsive elements (AREs) and other co-activator (SMaf) to induce the transcription of antioxidant and cytoprotective genes. B: Activation of caspase-3 is triggered by the induction of oxidative stress where ROS can impair the integrity of the mitochondrial membrane, releasing cytochrome C, which binds to apaf-1 and pro-caspase-9, releasing active caspase-9. Caspase-9 (active) cleaves inactive caspase-3 and converts it to active caspase-3. Active caspase-3 mediates the execution of programmed cell death. However, BET can form a strong interaction with the amino acid residues in the active site of caspase 3, thus suppressing its apoptotic function. Created by Arunsi Uche O. using BioRender, https://app.biorender.com/