关键词: 阿魏酸钠, Aβ25-35, TNF-α, p38 MAPK

Abstract: Objective To examine the effect and mechanism of sodium ferulate inhibiting p38MAPK in macrophage on neurotoxicity which was mediated by fribrilar -amyloid-induced. Methods The isolated peritoneal macropohages from mices were cultured . p38MAPK protein in nuclear extracts was analyzed by Western blot and production of tumor necrosis factor-α(TNF-α) was detected by ELISA. For neuron-macrophage co-cultures, Microtubute-associated protein-2(MAP-2) expression were detected by immunocytochemical technique. The level of LDH in the medium were measured. Results The production of TNF-α and p38MAPK protein in nuclear extracts increased significantly by incubation of Aβ25-35. LDH efflux in neuron-macrophage co-culture medium increased and MAP-2 expression decreased significantly(P<0.01). As to the sodium ferulate groups, however, the damages were dose-dependently eliminated (P<0.05). Conclusion Sodium ferulate could inhibit p38MAPK mediated by Aβ25-35 and decrease the production of TNF-α. Sodium ferulate could play a role in protecting the neurons against the impairments induced by Aβ25-35.

Key words: Sodium ferulate, Aβ25-35, TNF-α, p38MAPK