ABSTRACT
@#Alzheimer′s disease(AD)is an irreversible neurodegenerative disease. Main features in AD brains are abnormal deposition of amyloid-beta peptide(Aβ)in extracellular senile plaques(SP), intracellular neurofibrillary tangles(NFT)formed by hyperphosphorylated tau. The cause of AD is not clear. Oxidative stress is considered to be an important factor leading to the development of AD. Keap1-Nrf2-ARE signaling pathway is one of the most important defense mechanisms of antioxidant and/or electrophilic stress in the body. The activation of Keap1-Nrf2-ARE signaling pathway induces the transcription of a range of cytoprotective genes and reduces oxidative stress. This article outlines the therapeutic effect of flavonoids, phenols, carboxylic acids, esters and other Nrf2 activators on Alzheimer′s disease.
ABSTRACT
OBJECTIVE: Accumulating evidence suggests that oxidative stress plays a role in the pathophysiology of schizophrenia and that the potent antioxidants may be potential therapeutic drugs for schizophrenia. This study was undertaken to examine the effects of the potent antioxidant sulforaphane (SFN), found in cruciferous vegetables, on behavioral abnormalities (e.g., hyperlocomotion and prepulse inhibition [PPI] deficits) in mice after a single administration of the N-methyl-D-aspartate (NMDA)-receptor antagonist phencyclidine (PCP). METHODS: Effects of SFN (3, 10, and 30 mg/kg, intraperitoneally [i.p.]) on hyperlocomotion and PPI deficits in the adult male ddY mice after administration of PCP (3.0 mg/kg, subcutaneously [s.c.]) were examined. RESULTS: Administration of SFN (30 mg/kg, intraperitoneally [i.p.]), but not low doses (3 and 10 mg/kg, i.p.), significantly attenuated hyperlocomotion in mice after PCP administration (3.0 mg/kg, subcutaneously [s.c.]). Furthermore, administration of SFN (3, 10, and 30 mg/kg, i.p.) attenuated the PPI deficits in mice after PCP administration (3.0 mg/kg, s.c.) in a dose-dependent manner. CONCLUSION: These results suggest that SFN has antipsychotic activity in an animal model of schizophrenia. Therefore, it is likely that SFN may be a potential therapeutic drug for schizophrenia.