Involvement of Antioxidant and Prevention of Mitochondrial Dysfunction, Anti-Neuroinflammatory Effect and Anti-Apoptotic Effect: Betaine Ameliorates Haloperidol-Induced Orofacial Dyskinesia in Rats

With its pathophysiological characteristics strongly similar to patients with tardive dyskinesia (TD), haloperidol (HP)-induced neurotoxicity and orofacial (OD) in animal models have long been used study human TD. This aimed explore the potential protective effects of betaine (BT), a vital biochemical compound present plants, microorganisms, animals, various dietary sources. The focused on investigating impact BT rats, as well underlying neuroprotective mechanisms. To induce development OD, which is characterized by increased vacuous chewing movement (VCM) tongue protrusion (TP), rats were administered HP (1 mg/kg i.p.) for 21 consecutive days. was intraperitoneally (i.p.) at doses 30 100 mg/kg, 60 min later, successive On 21st day, after evaluating OD behavior, sacrificed, measurements taken assess nitrosative oxidative status, antioxidant capacity, mitochondrial function, neuroinflammation, apoptotic markers striatum. results demonstrated that (1) induced development, (2) found prevent most HP-induced OD; decrease stress levels; increase anti-oxidation power; dysfunction; reduce levels neuroinflammatory Our demonstrate against are credited prevention dysfunction, anti-neuroinflammatory effects, anti-apoptotic suggesting may be novel therapeutic candidate delaying or treating TD clinical settings. However, further studies will warranted extrapolate preclinical findings into better understanding role BT.