The protective effect of Borago Officinalis extract on amyloid ß (25-35)-induced long term potentiation disruption in the dentate gyrus of male rats.

Alzheimer's disease (AD) begins with impairment in synaptic functions before developing into later neurodegeneration and neural loss. In the present study we have examined the protective effects of Borago Officinalis (borage) extract on amyloid ß (Aß)--Induced long term potentiation (LTP) disruption in hippocampal dentate gyrus (DG). Wistar male rats received intrahippocampal (IHP) injection of the Aß (25-35) and borage extract throughout gestation (100 mg/kg). LTP in perforant path- DG synapses was assessed using electrophysiology method and field excitatory post- synaptic potential (fEPSP) slope and population spike (PS) amplitude were measured by 400 Hz tetanization. Finally, the total thiol content of hippocampus was measured using colorimetric reaction based on the Ellman's method. The results showed that Aß (25-35) significantly decreased fEPSP slope and SP amplitude comparing with the control and sham group, whereas borage extract administration increased these parameters compared to the Aß group. Aß induced a remarkable decrease in total thiol content of hippocampus and borage prevented the decrease of the hippocampal total sulfhydryl (SH) groups. This data suggest that Aß (25-35) can effectively inhibit LTP in the granular cells of the DG in hippocampus, and borage supplementation reverse the synaptic plasticity in DG following Aß treatment and that borage consumption may lead to an improvement of AD-induced cognitive dysfunction.

Attenuation of ecstasy-induced neurotoxicity by N-acetylcysteine.

UNLABELLED: Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) can lead to spatial memory impairments and hippocampal cell death. Numerous evidence indicates that the antioxidant N-acetylcysteine (NAC) exerts protective effects in the brain. The present study evaluates the effects of NAC on MDMA-induced neurotoxicity. METHODS: We intraperitoneally injected 28 adult male Sprague-Dawley rats (200-250 g) with either 0, 10 mg/kg of MDMA, or 10 mg/kg of MDMA plus 100 mg/kg of NAC. Spatial memory was assessed with a Morris Water Maze (MWM). At the end of the study, rats' brains were removed to study the structure and ultrastructure of CA1, and measure Bcl-2 and Bax expressions in the hippocampus. In the MWM, NAC treatment significantly attenuated the MDMA-induced increase in distance traveled (p < 0.05) and escape latency (p < 0.001). The decreased time spent in the target quadrant in MDMA-treated animals was attenuated by NAC (p < 0.01). NAC significantly protected against MDMA-induced apoptosis and the up- and down-regulation of Bax and Bcl-2, respectively. These data have suggested that NAC could protect against behavioral changes and apoptosis in the hippocampus following administration of MDMA. NAC might be useful for the treatment of neurotoxicity in MDMA users.

Influence of N-acetyl cysteine on beta-amyloid-induced Alzheimer's disease in a rat model: A behavioral and electrophysiological study.

Alzheimer's disease is an age-related neurodegenerative disorder characterized by a progressive decline in cognitive function due to the extracellular accumulation and deposition of beta-amyloid peptide (Aß). The purpose of this study was to evaluate the protective effect of N-acetyl cysteine (NAC) on learning and memory in an Aß-induced Alzheimer's disease model in adult male rats, using behavioral and electrophysiological methods Thirty-five rats were divided into five groups: control, sham-operated, Aß, Aß+NAC (1-14days), and Aß+NAC (14-28days). Learning and memory were evaluated behaviorally using the passive avoidance test and electrophysiologically by assessing hippocampal long-term potentiation, a cellular mechanism of learning and memory. Intrahippocampal Aß injections reduced step-through latency in the passive avoidance test, and decreased both the amplitude of hippocampal neuron population spikes and the slope of excitatory postsynaptic potentials, compared to the sham and control groups. Administration of NAC in rats receiving Aß alleviated the Aß-induced deficits in comparison to the Aß-only group. The results of this study suggest that NAC shows potential for treatment of Alzheimer's disease.

Protective effects of Borago officinalis extract on amyloid ß-peptide(25-35)-induced memory impairment in male rats: a behavioral study.

Alzheimer's disease (AD) is a neurodegenerative disorder and most common form of dementia that leads to memory impairment. In the present study we have examined the protective effects of Borago officinalis (borage) extract on Amyloid ß (A ß)-Induced memory impairment. Wistar male rats received intrahippocampal (IHP) injection of the A ß (25-35) and borage extract throughout gestation (100 mg/kg). Learning and memory functions in the rats were examined by the passive avoidance and the Morris water maze (MWM) tasks. Finally, the antioxidant capacity of hippocampus was measured using ferric ion reducing antioxidant power (FRAP) assay. The results showed that A ß (25-35) impaired step-through latency and time in dark compartment in passive avoidance task. In the MWM, A ß (25-35) significantly increased escape latency and traveled distance. Borage administration attenuated the A ß-induced memory impairment in both the passive avoidance and the MWM tasks. A ß induced a remarkable decrease in antioxidant power (FRAP value) of hippocampus and borage prevented the decrease of the hippocampal antioxidant status. This data suggests that borage could improve the learning impairment and oxidative damage in the hippocampal tissue following A ß treatment and that borage consumption may lead to an improvement of AD-induced cognitive dysfunction.