الفهرس 
Possible neurogenesis role of brain-derived neurotrophic factor (BDNF) in experimentally-induced Huntington disease (Code PO.3.4.3)
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Abstract
Morin, a potent antioxidant flavonoid, confers neuroprotection but its impact in combating Huntington Disease (HD) has not been tested before. Calpain is a protease enzyme that aids in the propagation of excitotoxicity has been shown to play a role in the pathogenesis of HD. Accordingly, this study aimed in assessing morin hydrate (MH) and the calpain inhibitor calpeptin (CP) neuroprotective potential in a 3-nitropropionic acid (3-NP)-induced HD model. HD rats were either left untreated or post-treated with morin hydrate, CP, or both for a week stating 14 days after the appearance of HD symptoms. Morin hydrate and/or CP post-treatment amendedmotor function assessed by the beam walking test and short- and long-term spatial memory determined by the Novel Object Recognition test with improved microscopic cortical architecture. All regimens were able to inhibit the cortical glutamate/calpain axis and KIDIN220 (ARMS) with the activation of the protein kinase B (AKT)/cAMP response element-binding protein(CREB)/ brain-derived neurotrophic factor(BDNF)/tropomyosin-related kinase receptor B (TrkB) trajectory. Additionally, morin hydrate and/or CP deactivated the nuclear factor (NF)-mB cue to abate both tumor necrosis factor-Ü(TNF-Ü) and interleukin-1Ý (IL-1Ý) pro-inflammatory cytokines, as well as lipid peroxidative response. Synergistic reduction in calpain and additive decreases in glutamate, KIDIN220 (ARMS), NF-mB/TNF-Ü and IL-1Ý with synergistic augmentation of the BDNF/TrkB/AKT occurred upon combining both morin hydrate and CP. In conclusion, morin hydrate, CP, and especially their combination, afford neuroprotection against HD through restrained glutamate excitotoxicity and NF-mB-mediated neuro-inflammation/oxidative stress with BDNF/TrkB/AKT hub activation dependent on calpain inhibition that was not related KIDIN220 (ARMS) suppression