TY - JOUR
T1 - MnTBAP, a synthetic metalloporphyrin, inhibits production of tumor necrosis factor-α in lipopolysaccharide-stimulated RAW 264.7 macrophages cells via inhibiting oxidative stress-mediating p38 and SAPK/JNK signaling
AU - Tumurkhuu, Gantsetseg
AU - Koide, Naoki
AU - Dagvadorj, Jargalsaikhan
AU - Hassan, Ferdaus
AU - Islam, Shamima
AU - Naiki, Yoshikazu
AU - Mori, Isamu
AU - Yoshida, Tomoaki
AU - Yokochi, Takashi
PY - 2007/3
Y1 - 2007/3
N2 - Antioxidants are able to inhibit inflammatory gene expression in response to lipopolysaccharide via down-regulating generation of intracellular reactive oxygen species (ROS) as second messengers. The effect of manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), a synthetic metalloporphyrin with antioxidant activity, on tumor necrosis factor (TNF)-α production in lipopolysaccharide-stimulated RAW 264.7 macrophage cells was examined. MnTBAP prevented the generation of intracellular ROS in lipopolysaccharide-stimulated RAW 264.7 cells and further inhibited lipopolysaccharide-induced TNF-α production. MnTBAP exclusively prevented the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase (SAPK/JNK) whereas it did not affect the phosphorylation and activation of nuclear factor-κB and extracellular signal regulated kinase 1/2. MnTBAP was suggested to inhibit lipopolysaccharide-induced TNF-α production by the prevention of intracellular ROS generation and subsequent inactivation of p38 MAPK and SAPK/JNK.
AB - Antioxidants are able to inhibit inflammatory gene expression in response to lipopolysaccharide via down-regulating generation of intracellular reactive oxygen species (ROS) as second messengers. The effect of manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), a synthetic metalloporphyrin with antioxidant activity, on tumor necrosis factor (TNF)-α production in lipopolysaccharide-stimulated RAW 264.7 macrophage cells was examined. MnTBAP prevented the generation of intracellular ROS in lipopolysaccharide-stimulated RAW 264.7 cells and further inhibited lipopolysaccharide-induced TNF-α production. MnTBAP exclusively prevented the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase (SAPK/JNK) whereas it did not affect the phosphorylation and activation of nuclear factor-κB and extracellular signal regulated kinase 1/2. MnTBAP was suggested to inhibit lipopolysaccharide-induced TNF-α production by the prevention of intracellular ROS generation and subsequent inactivation of p38 MAPK and SAPK/JNK.
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UR - http://www.scopus.com/inward/citedby.url?scp=33846974038&partnerID=8YFLogxK
U2 - 10.1111/j.1574-695X.2006.00203.x
DO - 10.1111/j.1574-695X.2006.00203.x
M3 - Article
C2 - 17227451
AN - SCOPUS:33846974038
SN - 0928-8244
VL - 49
SP - 304
EP - 311
JO - FEMS Immunology and Medical Microbiology
JF - FEMS Immunology and Medical Microbiology
IS - 2
ER -