Recent experimental and clinical reports support the fact that the
minocycline exhibits significant neuroprotective activity in
neurodegenerative diseases. However, its mechanism of neuroprotection is still far from our understanding. Besides,
minocycline does not always produce
neuroprotective effect. Therefore, this study has been designed to explore the possible mechanism of
minocycline in experimental model of HD in rats. Intrastriatal administration of
quinolinic acid caused a significant reduction in
body weight, motor dysfunction (impaired locomotor activity, rotarod performance, and beam walk test), oxidative damage (as evidenced by increase in lipid peroxidation,
nitrite concentration, and depletion of super
oxide dismutase and
catalase), increased TNF-α and
IL-6 levels as compared to the
sham-treated animals.
Minocycline (25, 50, and 100 mg/kg) treatment (for 21 days) significantly improved
body weight, locomotor activity, rotarod performance, balance beam walk performance, oxidative defense, attenuated TNF-α and
IL-6 levels as compared to
quinolinic-acid (QA)-treated animals. This study provides evidence that
minocycline might have
neuroprotective effect against QA-induced Huntington-like behavioral, biochemical alterations, and
neuroinflammation in rats.