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

Gantsetseg Tumurkhuu, Naoki Koide, Jargalsaikhan Dagvadorj, Ferdaus Hassan, Shamima Islam, Yoshikazu Naiki, Isamu Mori, Tomoaki Yoshida, Takashi Yokochi

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)304-311
Number of pages8
JournalFEMS Immunology and Medical Microbiology
Volume49
Issue number2
DOIs
Publication statusPublished - 03-2007

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

Fingerprint Dive into the research topics of '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'. Together they form a unique fingerprint.

Cite this