ABSTRACT
This study was to determine the protective effect of ω-3 polyunsaturated fatty acids (ω-3PUFAs) on MK-801-induced cognitive impairment in schizophrenia (SZ) rats and the underlying mechanism.A rat model of schizophrenia was induced by MK-801.The cognitive function of rats was assessed using a Morris water maze.The number of hippocampal neurons was measured by Nissl staining.The expression of CREB,p-CREB,BDNF,TrkB,p-TrkB,AKT,p-AKT,ERK,and p-ERK in the hippocampus of rats was detected by Western blotting.The results showed that ω-3PUFAs attenuated MK-801-induced cognitive,impairment and hippocampal neurons loss,reversed the injury of the CREB/BDNF/TrtB pathway induced by MK-801,and antagonized MK-801-induced down-regulation of p-AKT and p-ERK in the hippocampus of rats.In conclusion,ω-3PUFAs enhances the CREB/BDNF/TrkB pathway by activating ERK and AKT,thereby increasing the synaptic plasticity and decreashng neuron loss,and antagonizing MK-801-induced cognitive impairment in schizophrenic rats.
ABSTRACT
Helicobacter pylori (H.pylori) infection is a recognized risk factor of dementia,while its role and mechanism in Alzheimer disease (AD) remained unclarified.Our previous study has identified that injection of soluble H.pylori filtrate could induce AD-like pathologic changes and cognitive impairment in SD rats.In the present study,we further explored the effect of long-term stomach colonization of H.pylori bacteria on the brains of SD rats.The results showed that H.pylori bacteria gavage induced an efficient colonization of H.pylori in the stomach after four weeks.However,there was no significant change of tau phosphorylation at Thr205 (pT205),Thr231 (pT231),Ser396 (pS396) and Ser404 (pS404) sites in the hippocampus and cerebral cortex.The H.pylori-infected rats also showed no cognitive impairment.These observations may result from inefficient release of bacterial pathogenic factors or the overall lack of host inflammatory responses.We conclude that SD rat with long-term H.pylori colonization in the stomach is not a suitable animal model for exploring the effects of H.pylori infection on brain function in human beings;administration of bacterial filtrates may better reveal the systemic pathologic changes induced by bacterial infection in animals which show a negative host response to bacterial colonization.