The present study was aimed to investigate the effects of nizofenone administration on the chronic restraint stress-induced cognitive impairments in mice. Adult male mice were randomized into five groups: control group, nizofenone control group, chronic restraint stress group, and nizofenone treatment groups (3.0mg/kg and 9.0mg/kg). The changes of cognitive performances were examined by Morris water maze (MWM), open field and step-through tests. Our results showed that the cognitive performances in CRS group were markedly deteriorated, accompanied by noticeable alterations in oxidative parameters, acetylcholinesterase activity and catecholamines levels in the hippocampus and the prefrontal cortex. These changes could be reversed by nizofenone treatment. Moreover, CRS group showed higher corticosterone levels and lower catecholamines levels in the serum, which were reversed in the nizofenone treatment groups. Collectively, the present results suggested the potential of nizofenone in attenuating the CRS-induced cognitive impairments.

01 Apr 2003·European Journal of PharmacologyQ3 · MEDICINE

Pharmacological evidence for a correlation between hippocampal CA1 cell damage and hyperlocomotion following global cerebral ischemia in gerbils

Q3 · MEDICINE

Article

Author: Kiyotaka Katsuta ; Nobuya Matsuoka ; Noriko Ueyama ; Kazuo Umemura

Global ischemia, induced in Mongolian gerbils by bilateral occlusion of the carotid arteries for 5 min, produced a significant increase in locomotor activity at 1 day post-occlusion and a severe loss of hippocampal CA1 neurons at 4 days post-occlusion. To explore the pharmacological relationship between ischemia-induced hypermotility and CA1 cell death in the hippocampus, we evaluated the efficacy of diverse classes of putative neuroprotective agents for preventing hypermotility and delayed neuronal death. Administration of any drug 30 min before global ischemia dose-dependently, and with similar potency, ameliorated both hippocampal delayed neuronal death and locomotor hyperactivity, with a rank order: tacrolimus (FK506)>nizofenone>clonindine>dizocilpine (MK-801)>6-(1H-imidazol-1-yl)-7-nitro-2,3(1H,4H)-quinoxalinedione hydrochloride (YM90K)>phencyclidine>pentobarbital>2-(4-(p-fluorobenzoyl)-piperidin-1-yl)-2'-acetonaphthone hydrochloride (E-2001)>cis-(+/-)-4-phosphonomethyl-2-piperidine carboxylic acid (CGS19755)>3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]benzeneacetamide (U-50,488H)>piroxicam>eliprodil>vinpocetine. Furthermore, potencies of the protective effect on delayed neuronal death and inhibitory effects on hypermotility were closely correlated (r=0.98). These results suggest that post-ischemic CA1 injury and hypermotility share common mechanisms, and further imply that it is possible to predict the neuroprotective efficacy of drugs more easily by examining the inhibitory effects on post-ischemic hypermotility in global ischemia model in gerbils.

01 Nov 1999·Annals of the New York Academy of SciencesQ2 · CROSS-FIELD

Prevention of Neurodegeneration by a Neuroprotective Radical Scavenger

Q2 · CROSS-FIELD

Article

Author: Yasuda, H

Nizofenone (100 μM) inhibited the Fe²⁺/ascorbate-induced formation of malondialdehyde in brain or liver mitochondria completely.Incubation of neurons (N18-RE-105) with glutamate (5 mM, 24 h) resulted in a decrease in survival rate to ∼ 10%, the addition of nizofenone produced an increase in the surviving cells concentration-dependently.The antioxidative and neuroprotective activities of nizofenone were almost comparable to that of vitamin E.Nizofenone (10 mg/kg) prevented the postischemic increase in the hippocampus lactate levels and also prevented ischemia/perfusion-induced neuronal injury in the CA1 pyramidal cells.

100 Deals associated with Nizofenone

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KEGG	Wiki	ATC	Drug Bank
D08280	Nizofenone	N06BX10	DB13546

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