الفهرس | Only 14 pages are availabe for public view |
Abstract Huntington{u2019}s disease (HD) is a neurodegenerative disorder characterized by motor, cognitive and psychological symptoms. Noteworthy, the current treatments of HD are symptomatic. The current study investigated the neuroprotective mechanisms of dihydropyridine calcium channel blocker namely nimodipine against 3 nitropropionic acid (3NP)-induced HD model in rats. All rats were screened for motor abnormalities using the open field and rotarod tests. Also, memory impairment and stereotypical behavior were assessed in Morris water maze and open field, respectively. Besides, striatal and cortical contents of succinate dehydrogenase, neurotransmitters, oxidative stress biomarkers, inflammatory markers, survival and apoptotic biomarkers were estimated. In addition, histological and immunohistochemical examination of brain sections were investigated. Exposure to 3NP induces HD like symptoms possibly mediated, in part, via mitochondrial dysfunction, oxidative stress, excitotoxicity, inflammatory reactions in the brain. Nimodipine possesses neuroprotective abilities against HD most likely via a combination of several mechanisms such as calcium channel blockade, decrease in oxidative stress, mitigation of excitotoxicity besides reduction of inflammation and glial activation |