Abstract:

To investigate effects of APP17 peptides (βAmyloid precursor protein, APP, 319335 peptide fragment) on SAMP10(senescence accelerated mice/prone 10) learning memorizing, hippocampus tissue antioxidase activity, and the PI3K signal transduction pathway proteins in mice.  MethodLearning and memorizing variations were observed by a water maze test, malonaldehyde(MDA) contents in oxidized lipid degradation products were determined using the hydroxylamine and barbituric acid(TBA) method, erythrocuperin(SOD) activity using an xanthine oxidase method， and the PI3K signal transduction pathway proteins using immunohistochemical staining.  Results(1)Water maze results showed that evident learning and memorizing dysfunction existed in the model group. Ethological dysfunction in the APP17 peptide treatment group， which had no apparent differences compared with the normal controls， was evidently slighter than that in the model group. (2) SOD activity of mice hippocampus neurocyte mitochondria in the model group was manifestly degraded (P<0.01)，and MDA contents were markedly elevated compared with the normal controls (P<0.01). SOD activity was higher in the APP17 peptide treatment group than in the model group (P<0.05)，whereas MDA contents were lower in the APP17 peptide treatment group than in the model group(P<0.01). (3)Immunohistochemistry results showed that positive staining cell population of the relative protein TrkA, Akt/PKB, and bcl2 in mice hippocampus neurocyte PI3K signal transduction pathway was respectively reduced by 63%, 50% and 45% compared with the control group (P<0.01). After APP17 peptide therapy, expression of the abovementioned proteins was evidently upregulated (P<0.05)；expressions of NGF and CREB had no apparent differences(P>0.05). ConclusionLearning dysmnesia, reduced hippocampus tissue antioxidase activity, increased free radical metabolic product contents and abnormalexpression of PI3K signal transduction pathway protein existed in SAMP10(senescence accelerated mice/prone 10), which can be partially rectified by APP17.

Key words: Superoxide dismutase； Signal transduction； Amyloi d  betaprotein precursor 17 peptide； Mice