Abstract

In the present work, we found that the ethyl acetate-soluble fraction of Cnidium officinale MAKINO (COEA) decreased nitric oxide (NO) production in the lipopolysaccharide (LPS)-stimulated BV-2 and primary microglia and suppressed expression of inducible nitric oxide synthase (iNOS) in BV-2 cells with the same pattern of NO production. In addition, we showed that excessive NO production played an important role in neuronal cell death in LPS-treated rat hippocampal slice cultures. Our data suggest that the COEA inhibits neuronal cell death by reduction of excessive NO production in LPS-treated rat hippocampal slice cultures. The ethyl acetate-soluble fraction of C. officinale reduced propidium iodide uptake and NO production in cultured media at the same time.

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