Basic & Clinical Medicine ›› 2009, Vol. 29 ›› Issue (1): 42-46.

• 研究论文 • Previous Articles     Next Articles

Sodium ferulate inhibits neurons injury mediated by Aβ25-35-induced macrophage activation of mice

Su-yan YAO, Ying JING, De-yu ZHENG   

  1. Liaoning Medical College Liaoning Medical College Liaoning Medical College;Capital Medical University
  • Received:2008-01-14 Revised:2008-05-07 Online:2009-01-25 Published:2009-01-25
  • Contact: De-yu ZHENG

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

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