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Genipin inhibits the inflammatory response of rat brain microglial cells.

Abstract：

:Microglia are the prime effectors in immune and inflammatory responses of the central nervous system (CNS). Under pathological conditions, the activation of these cells helps restore CNS homeostasis. However, chronic microglial activation endangers neuronal survival through the release of various proinflammatory and neurotoxic factors. Thus, negative regulators of microglial activation have been considered as potential therapeutic candidates to target neurodegeneration, such as that in Alzheimer's and Parkinson's diseases. Genipin, the aglycon of geniposide found in gardenia fruit has long been considered for treatment of various disorders in traditional oriental medicine. Genipin has recently been reported to have diverse pharmacological functions, such as antimicrobial, antitumor, and anti-inflammatory effects. The specific aim of this study was to examine whether genipin represses brain microglial activation. Genipin was effective at inhibiting LPS-induced nitric oxide (NO) release from cultured rat brain microglial cells. Genipin reduced the LPS-stimulated production of tumor necrosis factor-alpha, interleukin-1beta, prostaglandin E(2), intracellular reactive oxygen species, and NF-kappaB activation. In addition, genipin reduced NO release from microglia stimulated with interferon-gamma and amyloid-beta. Both pretreatment and post-treatment of genipin to LPS-stimulated microglia were effective at decreasing NO release. Furthermore, genipin effectively inhibited microglial activation in a mouse model of brain inflammation. These results suggest that genipin provide neuroprotection by reducing the production of various neurotoxic molecules from activated microglia.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Nam KN,Choi YS,Jung HJ,Park GH,Park JM,Moon SK,Cho KH,Kang C,Kang I,Oh MS,Lee EH

doi

10.1016/j.intimp.2010.01.011

subject

Has Abstract

pub_date

2010-04-01 00:00:00

pages

493-9

issue

4

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(10)00038-X

journal_volume

10

pub_type

杂志文章

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