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Aim: To observe whether an amyloid β (Aβ)-induced increase in interleukin (IL)-1β was accompanied by an increase in the p38 mitogen-activated protein kinase (MAPK) pathway and a decrease in the cell survival pathway, and whether so-dium ferulate (SF) treatment was effective in preventing these Aβ-induced changes. Methods: Rats were injected intracerebroventricularly with Aβ_(25-35). Seven days after injection, immunohistochemical techniques for glial fibrillary acidic protein (GFAP) were used to determine the astrocyte infiltration and activation in hippo-campal CA1 areas. The expression of IL-1β, extracellular signal-regulated kinase (ERK), p38 MAPK, Akt/protein kinase B (PKB), Fas ligand and caspase-3 were determined by Western blotting. The caspase-3 activity was measured by clea-vage of the caspase-3 substrate (Ac-DEVD-pNA). Reverse transcription-polymerase chain reaction was used to analyze the changes in IL- 1βmRNA levels. Results:Intracerebroventricular injection of Aβ-(25-35) elicited astrocyte activation and infiltration and caused a strong inflammatory reaction characterized by increased IL-1β production and elevated levels of IL-1β mRNA. Increased IL-1β synthesis was accompanied by increased activation of p38 MAPK and downregulation of phospho-ERK and phospho-Akt/PKB in hippocampal CA regions prepared from Aβ-treated rats, leading to cell death as assessed by activa-tion of caspase-3. SF significantly prevented Aβ-induced increases in IL-Iβ and p38 MAPK activation and also Aβ-induced changes in phospho-ERK and phospho-Akt/PKB expression levels. Conclusion: SF prevents Aβ-induced neu-rotoxicity through suppression of p38 MAPK activation and upregulation of phospho-ERK and phospho-Akt/PKB expression.
Aim: To observe whether an amyloid β (Aβ)-induced increase in interleukin (IL)-1β was accompanied by an increase in the p38 mitogen-activated protein kinase (MAPK) pathway and a decrease in the cell survival pathway, and whether so -dium ferulate (SF) treatment was effectively in preventing these Aβ-induced changes. Methods: Rats were injected intracerebroventricularly with Aβ_(25-35). Seven days after injection, immunohistochemical techniques for glial fibrillary acidic proteins (GFAP) were used to determine The expression of IL-1β, extracellular signal-regulated kinase (ERK), p38 MAPK, Akt/protein kinase B (PKB), Fas ligand and caspase-3 were determined by Western. The astrocyte infiltration and activation in hippo-campal CA1 areas. Blotting. The caspase-3 activity was measured by clea-vage of the caspase-3 substrate (Ac-DEVD-pNA). Reverse transcription-polymerase chain reaction was used to analyze the changes in IL-1βmRNA levels. Results:Intracerebroventricular injection of Aβ-( 25-35) elicited astrocyte activation and infiltration and caused a strong inflammatory reaction characterized by increased IL-1β production and elevated levels of IL-1β mRNA. Increased IL-1β synthesis was accompanied by increased activation of p38 MAPK and downregulation of phospho-ERK And phospho-Akt/PKB in hippocampal CA regions prepared from Aβ-treated rats, leading to cell death as assessment by activa-tion of caspase-3. SF beautiful prevented Aβ-induced increases in IL-Iβ and p38 MAPK activation and also Aβ -induced changes in phospho-ERK and phospho-Akt/PKB expression levels. Conclusion: SF prevents Aβ-induced neu-rotoxicity through suppression of p38 MAPK activation and upregulation of phospho-ERK and phospho-Akt/PKB expression.