Neuroprotective Effects of

Introduction: Motor dysfunction severely reduces quality of life and is frequently linked to neurodegenerative disorders. By inhibiting succinate dehydrogenase, 3-nitropropionic acid (3- NP), a toxin, targets mitochondria and results in neurodegeneration. Neurons perish and lose energy as a result. Numerous models of neurodegenerative diseases with motor impairment have made use of this neurotoxic impact. Because of its phytoconstituents, the medicinal plant Materials & Methods: At 10 weeks of age, thirty Swiss male mice weighing between 19 and 35 g were split into three groups at random (n=10) and given the following treatments: Group II received 3-NP 15 mg/kg intraperitoneally (i.p.) for 5 days, group III received 3-NP 15 mg/kg (i.p.) and RV 20 mg/kg (p.o.), and group I received 2 mL of distilled water orally (p.o.) as the control. The beam walk test was used to assess motor coordination on the final day of the 21- day treatment. Following the neurobehavioral experiments, the animals were put to sleep, and blood was drawn by cardiac puncture. The levels of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured in the samples. 3-NP significantly reduced motor coordination, as demonstrated by the increase in foot slips, decreases in reversals, and line crossings during the beam walk test. Results: Concurrently, 3-NP generated oxidative stress, as demonstrated by increased levels of MDA and a decrease in levels of CAT, SOD, and GSH. Upon administration of RV, a considerable amelioration of the motor impairments and decreased oxidative stress generated by 3-NP occurred, which was indicated by an increase in the levels of CAT, SOD, and GPx and a reduction in MDA. Conclusion: In a 3-NP-induced model of motor dysfunction, the study's results demonstrated RV's neuroprotective capability and antioxidant qualities. They also point to RV as a possible treatment for movement disorders.