MAPK/ERK通路
活性氧
氧化应激
过氧化物还原蛋白
促炎细胞因子
信号转导
NFKB1型
NF-κB
一氧化氮合酶
化学
肿瘤坏死因子α
细胞生物学
炎症
癌症研究
生物
免疫学
生物化学
转录因子
酶
过氧化物酶
基因
作者
Hyung Jae Jeong,Meeyoung Park,Dae Won Kim,Eun Ji Ryu,Ji Yong,Hyun Ju,Sang Jin Kim,Hyeon Ji Yeo,Ji-Heon Jeong,Duk‐Soo Kim,Hyoung-Chun Kim,Eun Joo Shin,Eun Young Park,Jong Hoon Park,Hyeok Yil Kwon,Jinseu Park,Won Sik Eum,Soo Young Choi
标识
DOI:10.1016/j.intimp.2014.09.008
摘要
Excessive reactive oxygen species (ROS) production plays a crucial role in causing various diseases, including inflammatory disorders. The activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappaB (NF-κB) signaling is implicated in stimulating inflammatory response and cytokines. Peroxiredoxin 2 (Prx2) is a 2-cysteine (Cys) peroxiredoxin capable of removing endogenous hydrogen peroxide (H2O2). PEP-1 peptide, a protein transduction domain, consists of three domains which are used to transduce exogenous therapeutic proteins into cells. The correlation between effectively transduced PEP-1-Prx2 and ROS-mediated inflammatory response is not clear. In the present study, we investigated the protective effects of cell permeable PEP-1-Prx2 on oxidative stress-induced inflammatory activity in Raw 264.7 cells and in a mouse ear edema model after exposure to lipopolysaccharides (LPS) or 12-O-tetradecanoylphorbol-13-acetate (TPA). Transduced PEP-1-Prx2 suppressed intracellular ROS accumulation and inhibited the activity of MAPKs and NF-κB signaling that led to the suppression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and cytokines in LPS-induced Raw 264.7 cells and TPA-induced mouse ear edema model. Given these results, we propose that PEP-1-Prx2 has therapeutic potential in the prevention of inflammatory disorders.
科研通智能强力驱动
Strongly Powered by AbleSci AI