Mitigatory Roles of Asystasia Gangetica On Glutathione and Metabolic Enzyme Activities in The Cerebellum of Flunitrazepam-Induced Neurotoxicity in Wistar Rats

non-pharmaceutical use of drugs negatively impacts individuals, communities, and global public health. Flunitrazepam (FNZ), a benzodiazepine commonly associated with drug abuse and drug-facilitated sexual assault, exerts its effects by acting on GABA-A receptors. The brain is particularly vulnerable to oxidative damage due to its high oxygen consumption, relatively low antioxidant reserves, and abundance of polyunsaturated lipids. This study evaluated the protective effect of Asystasia gangetica aqueous leaf extract (AGLE) against FNZ-induced neurotoxicity in the cerebellum of Wistar rats. Forty adult male Wistar rats (200–230 g) were randomly allocated into four groups (n = 10 per group): Group 1 (control, distilled water), Group 2 (FNZ, 3 mg/kg bw), Group 3 (FNZ 3 mg/kg bw + AGLE 500 mg/kg bw), and Group 4 (AGLE 500 mg/kg bw). All treatments were administered orally for 21 days. Biochemical parameters assayed in cerebellar homogenates included reduced glutathione (GSH), glutathione peroxidase (GPx), oxidized glutathione (GSSG), GSH/GSSG ratio, glucose-6-phosphate dehydrogenase (G6PD), and lactate dehydrogenase (LDH). FNZ administration caused significant reductions in GSH, GPx, and GSH/GSSG ratio, and significant elevations in GSSG and LDH activity, consistent with oxidative stress and neuronal injury. G6PD activity showed a non-significant decrease. Co-administration of AGLE with FNZ substantially reversed these biochemical alterations toward control values. These findings demonstrate that A. gangetica aqueous leaf extract confers protective effects against FNZ-induced cerebellar oxidative neurotoxicity, and warrants further investigation as a potential adjunct therapeutic agent.