Portulaca oleracea Mitigates 3-Nitropropionic Acid-induced Motor Impairment, Mitochondrial Dysfunction and Free Radical Generation in Male Wistar Rats

The mitochondrial toxin 3-nitropropionic acid (3-NP) effectively induces behavioral changes and selective striatal lesions in rats mimicking clinical Huntington’s disease (HD). In the present study, behavioral tests and biochemical analysis were performed to explore the role of ethanolic extract of Portulaca oleracea (POEE) in the experimental animals of HD. Male wistar rats received an intraperitoneal injection of 3-NP (10 mg/kg) for 14 days. Simultaneously in treatment groups, the animals received POEE at a dose of 2 and 4 mg/kg along with 3-NP injection for a period of 14 days. The motor behavioral assessments were performed on days 5, 10 and 15. After the behavioral test on 15th day, the biochemical and histopathological parameters were performed. Administration of 3-NP resulted in body weight change, motor and memory impairments. 3-NP administration also causes marked oxidative stress by showing significantly increased levels of lipid peroxidation (LPO), nitric oxide (NO) and reduced activities of endogenous antioxidants. Further, it damages the mitochondrial complex enzyme succinate dehydrogenase (SDH) and elevated the acetylcholine esterase (AChE) activity. Treatment with POEE at 2 and 4 mg/kg bw doses significantly restored the body weight changes and behavioral impairment in 3-NP induced rats. Further, POEE significantly decreased the oxidative damages, restored the antioxidant enzymes activities and mitochondrial dysfunction. Histopathological sections of the striatal region showed the extent of neuronal loss in 3-NP induced rats and was restored upon POEE treatment. From the results, we suggest that POEE might be effective in clinical HD by virtue of its antioxidant and neuroprotective properties.