Fig. 15
Proposed mechanistic mode of action of betaine neuroprotective effect against NaF-induced neurotoxicity in male Wistar rats. BET confers protection to the cerebellum and cerebrum rats treated with NaF by enhancing redox balance and resolving inflammation. BET achieves this by suppressing the accumulation of ROS, as evidenced through increased levels of phase-1 antioxidants, including SOD, CAT, and GPx, which can detoxify O2.− and H2O2. Furthermore, BET increased the levels of phase-2 antioxidants GST, GSH, and TSH, crucial in detoxifying lipid hydroperoxides and primary oxidative products like MDA. Failure to upregulate these antioxidant molecules may result in MDA accumulation in rats’ cerebrum and cerebellum. Aside from regulating redox balance, BET also resolves inflammation by suppressing the levels of pro-inflammatory mediators while increasing the level of anti-inflammatory markers. Furthermore, BET prevented the manifestation of apoptosis in the cerebellum and cerebrum of rats by inhibiting the activity of caspase 3. Created by Arunsi Uche O. using BioRender, https://app.biorender.com/