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Allyl‐isothiocynate (AITC) ameliorates LPS induced NF‐κB mediated neuroinflammation
Author(s) -
Subedi Lalita,
Lee Taek Hwan,
Chae Jae Kyoung,
Venkatesan Ramu,
Kim Sun Yeou
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.lb158
Subject(s) - neuroprotection , neuroinflammation , microglia , pharmacology , nitric oxide synthase , nitric oxide , neurotrophin , chemistry , sh sy5y , neurotoxicity , neurotrophic factors , mapk/erk pathway , tumor necrosis factor alpha , nf κb , astrocyte , apoptosis , inflammation , signal transduction , toxicity , medicine , biology , immunology , neuroscience , biochemistry , cell culture , central nervous system , neuroblastoma , receptor , organic chemistry , genetics
Toxins‐induced microglial activation can initiate the inflammatory cascade in most of the neurodegenerative as well as neuroinflammatory conditions that leads to the neuronal cell death. Chronic activation of microglia is dangerous and the strategy to control the microglial over activation might be protective in neurodegenerative diseases. Natural compounds especially nutraceuticals are good examples for the treatment of such condition without cellular toxicity. In this study, we investigated the promising antineuroinflammatory activity as well as neuroprotective efficacy of allyl‐isothiocynate (AITC) from W. japonica against LPS activated BV‐2 cells and its toxicity to neuroblastoma cells called N2a cells. We evaluated the neurotrophic effect of AITC in neuronal astrocytes as well. AITC inhibited the LPS activated BV2 induced inducible nitric oxide synthase (iNOS), cyclooxygenase‐2 (COX‐2), nitric oxide (NO), prostaglandin E 2 (PGE 2 ), Tumor necrosis factor‐a (TNF‐a), interleukin‐6 (IL‐6), MAPK signaling, and NF‐κB mediated transcription. Additionally, AITC reduced the activated microglia induced neuronal toxicity via downregulating the neuronal apoptosis together with enhanced neurite outgrowth in neuronal cells. Furthermore AITC also increased the neurotrophins production through neuronal astrocytes. In conclusion, AITC might be a potential neuroprotective agent. Support or Funding Information This research was supported by High Value‐added Food Technology Development Program, Ministry of Agriculture, Food and Rural Affairs (114006041HD020)