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Effects Of H102on Inflammatory Reaction In The Brains Of APP Trans Genic Mice

Posted on:2011-01-24Degree:MasterType:Thesis
Country:ChinaCandidate:M SongFull Text:PDF
GTID:2284330467958135Subject:Physiology
Abstract/Summary:PDF Full Text Request
Objective:According to beta-amyloid (AP) cascade hypotyesis in Alzheimer’s disease (AD), this study is to observe effects of H102, a kind of β-Sheet breaker peptides, working on inflammatory reaction in the brains of APP transgenic mice, to look for the possible mechanism of H102in treating AD.Methods:APP695V717I transgenic mice were used in this study. There were three groups set called H102group, model group and a group of C57BL/6J mice with the same age and background was set as control group. Morris water maze test was used to screen learning and memory impairmed animals. Immunohistochemistry (IHC), western blot, inverted microscope and system of image pro-plus were used to determine protein expression of iNOS, IL-1β and TNF-a in brains of animals.Results:Morris water maze test showed that the escape latency of H102and control group were significantly shorter than model group, and original angle were signifcantly smaller than mode group, while the time stayed in the third quadrant were much more than model group (P<0.05, P<0.01). And the expression of iNOS, IL-1β and TNF-a detected by the methods of IHC and Western blot showed that lower content of these three proteins in the H102group and control group than model group (P<0.01), and there were no statistically significant difference between H102group and control group (P>0.05).Conclusion:H102can improve learning and memory performance of AD models. And effects of H102on inflammatory reaction in the brain of APP transgenic mouse was inhibitory. The possible mechanisms of that are explained as follow. H102has an ability to prevent accumulation and aggradation of Aβ, to decrease neurotoxicity of AP, moreover to depress the expression of inflammatory factors in AD brain. H102can also make microglia work positively to decrease the content and the expression of inflammatory factors and ameliorate the microenvironment to reduce inflammatory reaction and immunological response.
Keywords/Search Tags:Alzheimer’s disease, β-amyloid protein, H102Inducible nitric oxidesynthase, Interleukin-1β, Tumor necrosis factor-α
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