Inhibitory effect of FSLLRY-NH2 on inflammatory responses induced by hydrogen peroxide in HepG2 cells
- Authors
- Lee, Yeon Joo; Kim, Su Jin; Kwon, Kyoung Wan; Lee, Won Mo; Im, Wi Joon; Sohn, Uy Dong
- Issue Date
- Jul-2017
- Publisher
- PHARMACEUTICAL SOC KOREA
- Keywords
- HepG2; FSLLRY-NH2; PAR2; PAR2 antagonist
- Citation
- ARCHIVES OF PHARMACAL RESEARCH, v.40, no.7, pp 854 - 863
- Pages
- 10
- Journal Title
- ARCHIVES OF PHARMACAL RESEARCH
- Volume
- 40
- Number
- 7
- Start Page
- 854
- End Page
- 863
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/4300
- DOI
- 10.1007/s12272-017-0927-9
- ISSN
- 0253-6269
1976-3786
- Abstract
- Proteinase activated receptor 2 (PAR2), which is localized in the GI tract, the respiratory system, and the kidney tubules is a G protein-coupled receptor associated with inflammation, metabolism, and disease. The aim of this study was to explore the role of PAR2 in hydrogen peroxide (H2O2)-induced HepG2 cells by using FSLLRY-NH2 a PAR2 antagonist. H2O2 treatment resulted in induction of PAR2 in esophageal, gastric, and liver cells, with the most robust response being in HepG2 cells. Furthermore, this effect was dose-dependent in HepG2 cells. Treatment with H2O2 at concentrations above 400 mu M for 24 h also reduced HepG2 cell viability. H2O2 treatment increased both the protein and mRNA levels of IL-1 beta, IL-8, and TNF-alpha, as well as those of SAPK/JNK. The increased levels of these pro-inflammatory genes and SAPK/JNK induced by H2O2 were attenuated in a dose-dependent manner when cells were co-treated with H2O2 and FSLLRY-NH2. In summary, the PAR2 antagonist peptide, FSLLRY-NH2, reduces the level of the pro-inflammatory genes IL-8, IL-1 beta, and TNF-alpha induced by H2O2, through the SAPK/JNK pathways in HepG2 cells. These data suggest that a PAR2 antagonist could be an anti-inflammatory agent in HepG2 cells.
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