Tat-GSTpi suppresses inflammatory responses by regulating ROS/MAPKs/apoptosis signaling pathways

  • Yeo, Eun Ji; 
  • Shin, Min Jea; 
  • Youn, Gi Soo; 
  • Park, Jung Hwan; 
  • Yeo, Hyeon Ji; 
  • ... Kim, Duk-Soo; 
  • 외 12명
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초록

Glutathione S-transferase pi (GSTpi) is a phase II detoxifying enzyme that plays key roles in cellular processes. In a previous study, we have reported that cell permeable Tat-GSTpi can protect dopaminergic neurons against cell death. However, the precise roles of GSTpi in inflammation remain to be elucidated. Thus, the objective of present study is to investigate the one of plausible protective mechanism involved anti-inflammatory effect of GSTpi using lipopolysaccharide (LPS)- and phages and an animal model. It was revealed that cell permeable Tat-GSTpi fusion protein markedly reduced reactive oxygen species (ROS) and DNA injury in LPS-treated cells and transduced protein showed not only inhibition of the regulation of mitogen-activated protein kinase (MAPK) and Caspase-9, but also decrease of COX-2 and iNOS expressions. Furthermore, Tat-GSTpi ameliorated skin inflammation in an animal model by inhibition the COX-2, iNOS expression and cytokines. Those results indicate that GSTpi plays a role in antagonizing LPS- and TPA-induced inflammation, suggesting GSTpi has the potential to serve as a therapeutic treatment for inflammatory related diseases. [BMB Reports 2025; 58(6): 238-243]

키워드

Inflammation; MAPK; Protein therapy; ROS; Tat-GSTpi; NF-KAPPA-B; NITRIC-OXIDE SYNTHASE; INDUCED SKIN INFLAMMATION; S-TRANSFERASE P1-1; OXIDATIVE STRESS; CELL-PROLIFERATION; MICROGLIAL CELLS; EXPRESSION; MAPK; ACTIVATION
제목
Tat-GSTpi suppresses inflammatory responses by regulating ROS/MAPKs/apoptosis signaling pathways
저자
Yeo, Eun Ji; Shin, Min Jea; Youn, Gi Soo; Park, Jung Hwan; Yeo, Hyeon Ji; Kwon, Hyun Jung; Choi, Yeon Joo; Lee, Lee Re; Kim, Na Yeon; Kwon, Su Yeon; Kim, Su Min; Lee, Keun Wook; Park, Jong Kook; Lee, Chan Hee; Kim, Dae Won; Kim, Duk-Soo; Eum, Won Sik; Choi, Soo Young
DOI
10.5483/BMBRep.2024-0114
발행일
2025-12
유형
Article
저널명
BMB Reports
권
58
호
6
페이지
238 ~ 243