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PEP-1-GLRX1 Protein Exhibits Anti-Inflammatory Effects by Inhibiting the Activation of MAPK and NF-κB Pathways in Raw 264.7 Cells

BMB Reports 2020년 53권 2호 p.106 ~ 111
 ( Shin Min-Jea ) - Hallym University Department of Biomedical Science

김대원 ( Kim Dae-Won ) - Gangneung-Wonju National University College of Dentistry Department of Biochemistry and Molecular Biology
최연주 ( Choi Yeon-Joo ) - Hallym University Department of Biomedical Science
 ( Cha Hyun-Ju ) - Hallym University Department of Biomedical Science
 ( Lee Sung-Ho ) - Hallym University Department of Biomedical Science
이승호 ( Lee Sung-Hou ) - Sangmyung University Department of Green Chemical Engineering
박진서 ( Park Jin-Seu ) - Hallym University Department of Biomedical Science
한규형 ( Han Kyu-Hyung ) - Hallym University Department of Biomedical Science
엄원식 ( Eum Won-Sik ) - Hallym University Department of Biomedical Science
최수영 ( Choi Soo-Young ) - Hallym University Department of Biomedical Science

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.

키워드

Inflammation; MAPK; NF-κB; PEP-1-GLRX1; Protein therapy
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