TY - JOUR
T1 - Inhibitory effect of the gut microbial linoleic acid metabolites, 10-oxo-trans-11-octadecenoic acid and 10-hydroxy-cis-12-octadecenoic acid, on BV-2 microglial cell activation
AU - Ikeguchi, Shiori
AU - Izumi, Yasuhiko
AU - Kitamura, Nahoko
AU - Kishino, Shigenobu
AU - Ogawa, Jun
AU - Akaike, Akinori
AU - Kume, Toshiaki
N1 - Publisher Copyright:
© 2018 The Authors
PY - 2018/9
Y1 - 2018/9
N2 - 10-oxo-trans-11-octadecenoic acid (KetoC) and 10-hydroxy-cis-12-octadecenoic acid (HYA) are long-chain fatty acids generated from linoleic acid by the gut lactic acid bacterium Lactobacillus plantarum. These fatty acids have been reported to have anti-inflammatory activity in the intestine. However, little is known about their effects in the brain. In this study, we aimed to investigate the effects of these fatty acids on lipopolysaccharide (LPS)-induced inflammatory processes in mouse microglial cells (BV-2 cells). KetoC and HYA inhibited LPS-induced nitric oxide (NO) production and suppressed the expression of inducible NO synthase in BV-2 cells. NO changes in these inhibitory effects were observed with AH7614, a G-protein coupled receptor 120 antagonist, or the peroxisome proliferator-activated receptors antagonists, GW6471 and GW9662. In addition, KetoC and HYA did not inhibit translocation of p65, a subunit of NF-κB, or IκB degradation. Similarly, no effect on p38 or JNK phosphorylation was observed. However, KetoC and HYA were found to inhibit ERK phosphorylation induced by LPS, suggesting that these fatty acids may exert their anti-inflammatory effects through the inhibition of ERK activation in microglial cells.
AB - 10-oxo-trans-11-octadecenoic acid (KetoC) and 10-hydroxy-cis-12-octadecenoic acid (HYA) are long-chain fatty acids generated from linoleic acid by the gut lactic acid bacterium Lactobacillus plantarum. These fatty acids have been reported to have anti-inflammatory activity in the intestine. However, little is known about their effects in the brain. In this study, we aimed to investigate the effects of these fatty acids on lipopolysaccharide (LPS)-induced inflammatory processes in mouse microglial cells (BV-2 cells). KetoC and HYA inhibited LPS-induced nitric oxide (NO) production and suppressed the expression of inducible NO synthase in BV-2 cells. NO changes in these inhibitory effects were observed with AH7614, a G-protein coupled receptor 120 antagonist, or the peroxisome proliferator-activated receptors antagonists, GW6471 and GW9662. In addition, KetoC and HYA did not inhibit translocation of p65, a subunit of NF-κB, or IκB degradation. Similarly, no effect on p38 or JNK phosphorylation was observed. However, KetoC and HYA were found to inhibit ERK phosphorylation induced by LPS, suggesting that these fatty acids may exert their anti-inflammatory effects through the inhibition of ERK activation in microglial cells.
KW - Gut bacterium
KW - Inflammation
KW - MAPKs
KW - Microglia
KW - Polyunsaturated fatty acids
UR - http://www.scopus.com/inward/record.url?scp=85053731406&partnerID=8YFLogxK
U2 - 10.1016/j.jphs.2018.06.015
DO - 10.1016/j.jphs.2018.06.015
M3 - 学術論文
C2 - 30243517
AN - SCOPUS:85053731406
SN - 1347-8613
VL - 138
SP - 9
EP - 15
JO - Journal of Pharmacological Sciences
JF - Journal of Pharmacological Sciences
IS - 1
ER -