PMID- 26136104
OWN - NLM
STAT- MEDLINE
DCOM- 20160509
LR  - 20150808
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 36
IP  - 3
DP  - 2015 Sep
TI  - YCG063 inhibits Pseudomonas aeruginosa LPS-induced inflammation in human retinal 
      pigment epithelial cells through the TLR2-mediated AKT/NF-kappaB pathway and 
      ROS-independent pathways.
PG  - 808-16
LID - 10.3892/ijmm.2015.2266 [doi]
AB  - YCG063 is known as an inhibitor of reactive oxygen species (ROS); however, its 
      intracellular mechanisms of action remain poorly understood. In the present 
      study, we investigated the effects of YCG063 on the inflammatory response of 
      Pseudomonas aeruginosa lipopolysaccharide (PA-LPS)‑stimulated human retinal 
      pigment epithelial cells (RPE cells). Human adult RPE cells (ARPE‑19) were 
      stimulated with PA-LPS. We then investigated the LPS-induced expression of 
      several inflammatory mediators, such as interleukin (IL)-6, IL-8, monocyte 
      chemoattractant protein-1 (MCP-1) and intracellular adhesion molecule-1 (ICAM-1) 
      in the ARPE-19 cells. We performed an enzyme-linked immunosorbent assay (ELISA), 
      western blot analysis, electrophoretic mobility shift assay (EMSA) and 
      fluorescence-activated cell sorting (FACS) to elucidate the mechanisms involved 
      in the anti-inflammatory effects of YCG063 in the PA-LPS-stimulated cells. The 
      results revealed that treatment with YCG063 significantly inhibited the levels of 
      IL-6, IL-8, MCP-1 and ICAM-1 in the PA-LPS-stimulated ARPE-19 cells. YCG063 also 
      markedly inhibited the phosphorylation of AKT in the PA‑LPS-stimulated cells. In 
      addition, the activation of nuclear factor-kappaB (NF-kappaB) was also attenuated 
      folllowing treatment with YCG063. ROS were not generated in the PA-LPS-stimulated 
      cells. In conclusion, our data indicate that YCG063 may prove to be a potential 
      protective agent against inflammation, possibly through the downregulation of 
      Toll‑like receptor 2 (TLR2) and the AKT-dependent NF-kappaB activation pathway in 
      PA-LPS-stimulated ARPE-19 cells. Furthermore, this anti-inflammatory activity 
      occurred through ROS-independent signaling pathways.
FAU - Paeng, Sung Hwa
AU  - Paeng SH
AD  - Department of Neurosurgery, Busan Paik Hospital, Inje University College of 
      Medicine, Busan, Republic of Korea.
FAU - Park, Won Sun
AU  - Park WS
AD  - Department of Physiology, Kangwon National University School of Medicine, 
      Chuncheon, Gangwon, Republic of Korea.
FAU - Jung, Won-Kyo
AU  - Jung WK
AD  - Department of Biomedical Engineering, and Center for Marine-Integrated Biomedical 
      Technology (BK21 Plus), Pukyong National University, Busan, Republic of Korea.
FAU - Lee, Dae-Sung
AU  - Lee DS
AD  - Marine Biodiversity Institute of Korea, Seocheon, Chungcheongnam-do, Republic of 
      Korea.
FAU - Kim, Gi-Young
AU  - Kim GY
AD  - Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National 
      University, Jeju, Republic of Korea.
FAU - Choi, Yung Hyun
AU  - Choi YH
AD  - Department of Biochemistry, College of Oriental Medicine, Dongeui University, 
      Busan, Republic of Korea.
FAU - Seo, Su-Kil
AU  - Seo SK
AD  - Department of Microbiology, Inje University College of Medicine, Busan, Republic 
      of Korea.
FAU - Jang, Won Hee
AU  - Jang WH
AD  - Department of Biochemistry, Inje University College of Medicine, Busan, Republic 
      of Korea.
FAU - Choi, Jung Sik
AU  - Choi JS
AD  - Department of Internal Medicine, Busan Paik Hospital, Inje University College of 
      Medicine, Busan, Republic of Korea.
FAU - Lee, Young-Min
AU  - Lee YM
AD  - Department of Internal Medicine, Busan Paik Hospital, Inje University College of 
      Medicine, Busan, Republic of Korea.
FAU - Park, Saegwang
AU  - Park S
AD  - Department of Microbiology, Inje University College of Medicine, Busan, Republic 
      of Korea.
FAU - Choi, Il-Whan
AU  - Choi IW
AD  - Department of Microbiology, Inje University College of Medicine, Busan, Republic 
      of Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150630
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Hydrazones)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitroimidazoles)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (YCG 063)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Adult
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Humans
MH  - Hydrazones/*pharmacology
MH  - Inflammation/*drug therapy/immunology/*microbiology
MH  - Lipopolysaccharides/*immunology
MH  - NF-kappa B/immunology
MH  - Nitroimidazoles/*pharmacology
MH  - Proto-Oncogene Proteins c-akt/immunology
MH  - Pseudomonas aeruginosa/*immunology
MH  - Reactive Oxygen Species/immunology
MH  - Retinal Pigment Epithelium/cytology/*drug effects/immunology/microbiology
MH  - Signal Transduction/drug effects
MH  - Toll-Like Receptor 2/immunology
EDAT- 2015/07/03 06:00
MHDA- 2016/05/10 06:00
CRDT- 2015/07/03 06:00
PHST- 2014/11/12 00:00 [received]
PHST- 2015/06/22 00:00 [accepted]
PHST- 2015/07/03 06:00 [entrez]
PHST- 2015/07/03 06:00 [pubmed]
PHST- 2016/05/10 06:00 [medline]
AID - 10.3892/ijmm.2015.2266 [doi]
PST - ppublish
SO  - Int J Mol Med. 2015 Sep;36(3):808-16. doi: 10.3892/ijmm.2015.2266. Epub 2015 Jun 
      30.