PEP-1-GLRX1 protein exhibits anti-inflammatory effects by inhibiting the activation of MAPK and NF-κB pathways in Raw 264.7 cells.

Abstract

Glutaredoxin 1 (GLRX1) has been recognized as an important regulator of redox signaling. Although GLRX1 plays an essential role in cell survival as an antioxidant protein, the function of GLRX1 protein in inflammatory response is still under investigation. Therefore, we wanted to know whether transduced PEP-1-GLRX1 protein inhibits lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. In LPS-exposed Raw 264.7 cells, PEP-1-GLRX1 inhibited cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), activation of mitogen activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-κB) expression levels. In a TPA-induced mouse-ear edema model, topically applied PEP-1-GLRX1 transduced into ear tissues and significantly ameliorated ear edema. Our data reveal that PEP-1-GLRX1 attenuates inflammation in vitro and in vivo, suggesting that PEP-1-GLRX1 may be a potential therapeutic protein for inflammatory diseases. [BMB Reports 2020; 53(2): 106-111].

• Authors: Min Jea Shin, Dae Won Kim, Yeon Joo Choi, Hyun Ju Cha, Sung Ho Lee, Jinseu Park, Kyu Hyung Han, Won Sik Eum, Soo Young Choi
• Journal: BMB reports (BMB Rep) Vol. 53 Issue 2 Pg. 106-111 (Feb 2020) ISSN: 1976-670X [Electronic] Korea (South)
• PMID: 31964467 (Publication Type: Journal Article)

Chemical References

• Anti-Inflammatory Agents
• Cyclooxygenase 2 Inhibitors
• Glutaredoxins
• Lipopolysaccharides
• NF-kappa B
• Pep-1 peptide
• Peptides
• Cysteamine
• Nitric Oxide Synthase Type II
• Cyclooxygenase 2
• Mitogen-Activated Protein Kinases
• Tetradecanoylphorbol Acetate

Topics

• Animals
• Anti-Inflammatory Agents (pharmacology)
• Cyclooxygenase 2 (metabolism)
• Cyclooxygenase 2 Inhibitors (pharmacology)
• Cysteamine (analogs & derivatives)
• Edema (chemically induced, metabolism, therapy)
• Glutaredoxins (pharmacology)
• Inflammation (metabolism)
• Lipopolysaccharides (pharmacology)
• Male
• Mice
• Mice, Inbred ICR
• Mitogen-Activated Protein Kinases (antagonists & inhibitors, metabolism)
• NF-kappa B (metabolism)
• Nitric Oxide Synthase Type II (antagonists & inhibitors, metabolism)
• Peptides
• Phosphorylation
• RAW 264.7 Cells
• Signal Transduction (drug effects)
• Tetradecanoylphorbol Acetate (pharmacology)