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Methanol extract of Ficus leaf inhibits the production of nitric oxide and proinflammatory cytokines in LPS‐stimulated microglia via the MAPK pathway
Author(s) -
Jung Hyo Won,
Son Hye Young,
Minh Chau Van,
Kim Young Ho,
Park YongKi
Publication year - 2008
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2442
Subject(s) - proinflammatory cytokine , nitric oxide , mapk/erk pathway , nitric oxide synthase , tumor necrosis factor alpha , microglia , p38 mitogen activated protein kinases , kinase , microbiology and biotechnology , biology , chemistry , pharmacology , immunology , inflammation , endocrinology
Abstract Excessive production of inflammatory mediators, nitric oxide (NO) and proinflammatory cytokines from activated microglia has been implicated in neurodegeneration in human brain diseases. Recently, it seems possible that treatment with antiinflammatory agents, including Oriental medicinal plants, might delay the progression of neurodegeneration through the inhibition of microglial activation. The present study evaluated the effect of a methanol extract of Ficus religiosa leaf (MFL) on lipopolysaccharide (LPS)‐induced production of NO and proinflammatory cytokines, such as tumor necrosis factor‐alpha (TNF‐ α ), interleukin‐beta (IL‐1 β ) and IL‐6 in BV‐2 cells, a mouse microglial line. MFL inhibited LPS‐induced production of NO and proinflammatory cytokines in a dose‐dependent manner. MFL also attenuated the expression of mRNA and proteins of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines, suggesting the blockage of transcription levels, respectively. The molecular mechanism of MFL‐mediated attenuation underlies the down‐regulation of the extracellular signal‐regulated kinase (ERK), c‐Jun N ‐terminal kinase (JNK) and p38 mitogen‐activated protein kinase (MAPK) signaling pathway, and suppresses the nuclear factor kappaB (NF‐ κ B) activation. The results suggest that MFL exhibits antiinflammatory properties in LPS‐induced activation of BV2 microglial cells, and that might have a therapeutic potential for various neurodegenerative diseases. Copyright © 2008 John Wiley & Sons, Ltd.