Anti-Huntington's Effect of Butin in 3-Nitropropionic Acid-Treated Rats: Possible Mechanism of Action.

Butin has a strong antioxidant plus anti-inflammatory action and it is reported to be protective in oxidative stress-induced mitochondrial dysfunction. Butin has been shown to protect the mouse hippocampus HT22 cells from glutamate-induced neurotoxicity. The current investigation was planned to assess anti-Huntington's effect of butin in 3-nitropropionic acid-treated rats. A total of 32 Wistar rats (200-240 g) were equally segregated into four groups. Groups I and II were treated with vehicle (0.3 ml/100 g) and groups III and IV received butin 25 and 50 mg/kg for 15 days. Daily 1 h post above oral treatments, 3 ml/kg of normal saline was injected (i.p.) to group I animals and 10 mg/kg of 3-NP was injected (i.p.) to II and IV groups for 15 days. During the experimental schedule, behavioral tests were conducted for animals. On day 15, after behavioral parameters, animals were sacrificed and brains were removed for biochemical tests. Systemic administration of 3-NP induced neurobehavioral deficits which resulted in reduced spontaneous locomotor activity, motor incoordination, learning ability, and memory in the animals. Moreover, 3-NP depleted endogenous antioxidants (GSH, catalase, and SOD), mitochondrial complexes activities (I, II, IV, and MTT assay), elevated LDH, MDA, nitrite, and AchE. Administration of butin significantly improved neurobehavioral impairments, nitrative and oxidative stress, activities of mitochondrial enzyme complex, and reduced AchE levels in rat brain.