| Objective Our study was to determine the effect of β-1,3-galactosyltransferase II on senescence and soluble Aβ1-42-mediated neurodegenerative changes and its effect on Notch1,to clarify β-1,3-galactosyltransferase Ⅱ in neurodegenerative changes and its mechanism.Our results will provide a theoretical basis for further study glycosyltransferase on age-related neurodegenerative diseases for prevention,diagnosis and treatment..Methods Animals group: Mice were divided into two groups,the normal aged model mice(24 months old)and the young control group(3 months old).The expression of β-1,3-galactosyltransferase Ⅱ protein,neuron dendritic marker MAP2 and Notch signaling pathway were detected by immunohistochemical staining and Western Blotting.Cells group: Cortical cells were prepared from 17 days CD-1 mice embryonic cerebral cortex and were randomly divided into six groups,control group;Aβ1-42 group;β-1,3-galt2 c DNA group;Aβ1-42 + β-1,3-galt2 c DNA group;β-1,3-galt2 si RNA group;Aβ1-42 + β-1,3-galt2 si RNA group.RT-PCR and immunohistochemical staining were used to verify the effect of β-1,3-galactosyltransferase Ⅱ c DNA and si RNA transfection.Immunohistochemistry was used to observe the expression of MAP2 and the expression of SNAP25 and Notch1 in the neurons ofβ-1,3-galactosyltransferase Ⅱ overexpression and low expression.Results 1.β-1,3-galt2 expression was decreased in the elderly cerebral cortex.2.Notch1 expression was decreased in the elderly mice cerebral cortex.3,Soluble Aβ1-42 reduce the expression of β-1,3-galt2 gene and protein in cortex cells,and also reduce the expression of Notch1.4,β-1,3-galt2 overexpression can improve the effect of soluble Aβ1-42 on dendritic marker protein MAP2 and synaptic related protein SNAP25.5,β-1,3-galt2 overexpression or low expression can respectively improve or aggravate the effect of soluble Aβ1-42 on Notch1.Conclusions 1,β-1,3-galactosyltransferase Ⅱ plays an important role in senescence and soluble Aβ1-42-mediated neurodegenerative changes.2,β-1,3-galactosyltransferase Ⅱ may play its role in neurodegenerative changes in neuronal protection through the Notch signaling pathway. |