Huntington’s disease (HD) is a devastating neurodegenerative disorder with no cure till date. Many genetic or chemically
induced models have been developed in rodents to study the disease. 3-Nitropropionic (3-NP) acid is a well-known
neurotoxin to induce Huntington’s disease (HD) in rodents. It replicates the pathology of HD by causing oxidative stress.
Esculetin is a natural compound, a coumarin, known to have neuroprotective effect in a mouse model of Parkinson’s
disease. In the present study, the neuroprotective effect of esculetin on 3-NP induced oxidative stress in rat striatum was
determined by behavioral and biochemical parameters. Rats were induced with 3-NP (10mg/kg) intraperitoneally for 14
days and rats induced with 3-NP were treated with esculetin (25mg/kg and 50mg/kg) for 14 days. Esculetin attenuated the
behaviour of rats in morris water maze, open field, forced swim, narrow beam walk and grip strength test. Biochemical
effect of esculetin was also studied on oxidative stress markers, SDH and acetylcholinesterase. Esculetin treatment
alleviated the increased values of acetylcholinesterase, protein carbonyls and lipid peroxidation. On treatment with
esculetin, we observed that the levels of SOD, GSH, catalase, glutathione peroxidase, SDH were increased. The present
study shows that the antioxidant activity of esculetin may be responsible for its neuroprotective activity against 3-
nitropropionic acid induced neurotoxicity in rats
Neuroprotective effect of solanesol against 3-nitropropionic acid-induced Huntington's disease-like behavioral, biochemical, and cellular alterations: Restoration of coenzyme-Q10-mediated mitochondrial dysfunction
