Effects of sodium ferulate on A?_(25-35)-induced cognitive deficits and expression of IL-1? and p38MAPK in rats
- VernacularTitle:阿魏酸钠对抗A?(25-35)致大鼠学习记忆障碍与IL-1?和p38MAPK表达的相关性探讨
- Author:
Ying JIN
;
Enzhi YAN
;
Ying FAN
;
Zhimin QI
;
Cuifen BAO
- Publication Type:Journal Article
- Keywords:
amyloid beta-protein;
inflammation;
p38MAP kinase;
sodium ferulate
- From:
Chinese Pharmacological Bulletin
1986;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To study the effects of sodium ferulate on A?induced cognitive deficits and expressions of IL-1? and phospho-p38MAPK proteins.Methods Alzheimers disease model of rats was produced by intracerebroventricular injection of A?_(25-35)(10 ?g,once).Morris water maze was used to measure spatial memory performance.Nissl staining and immunohistochemical technique for glial fibrillary acidic protein(GFAP) were employed to determine the morphology of pyramidal neurons and astrocyte infiltration in hippocmpal CA1 regions.The levels of phospho-p38MAPK and IL-1? were determined by Western blot and ELISA method.Reverse transcription-PCR analysis showed changes in FasL mRNA.Results Intracerebroventricular injection of A?_(25-35)in rats resulted in spatial memory impairments shown by longer escape latency and decreased percentage of time spent in the target quadrant.These behavioral dysfunctions were accompanied by astrocyte activation and infiltration,increased IL-1? production and elevated FasL mRNA level,the loss of pyramidal neurons in hippocampal CA1,and the increase of phosphorylated p38MAPK.Oral administration of sodium ferulate(50,100,250 mg?kg~(-1)daily) and ibuprofen 15 mg?kg~(-1)daily markedly improved the memory impairment,attenuated pyramidal neuronal damage,and reversed the A?-induced increases in IL-1? and p38MAPK activation.Conclusion sodium ferulate prevents A?-induced neurotoxicity through suppressions of inflammatory response and the activation of p38MAPK.
