PMID- 35437426
OWN - NLM
STAT- MEDLINE
DCOM- 20220420
LR  - 20220716
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2022
DP  - 2022
TI  - Chlorogenic Acid as a Positive Regulator in LPS-PG-Induced Inflammation via 
      TLR4/MyD88-Mediated NF-kappaB and PI3K/MAPK Signaling Cascades in Human Gingival 
      Fibroblasts.
PG  - 2127642
LID - 10.1155/2022/2127642 [doi]
LID - 2127642
AB  - Gingival inflammation is one of the main causes that can be related to various 
      periodontal diseases. Human gingival fibroblast (HGF) is the major constituent in 
      periodontal connective tissue and secretes various inflammatory mediators, such 
      as nitric oxide (NO) and prostaglandin E(2) (PGE(2)), upon lipopolysaccharide 
      stimulation. This study is aimed at investigating the anti-inflammatory mechanism 
      of chlorogenic acid (CGA) on Porphyromonas gingivalis LPS- (LPS-PG-) stimulated 
      HGF-1 cells. The concentration of NO and PGE(2), as well as their responsible 
      enzymes, inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2), was analyzed 
      by Griess reaction, ELISA, and western blot analysis. LPS-PG sharply elevated the 
      production and protein expression of inflammatory mediators, which were 
      significantly attenuated by CGA treatment in a dose-dependent manner. CGA 
      treatment also suppressed activation of Toll-like receptor 4 (TLR4)/myeloid 
      differentiation primary response gene 88 (MyD88) and nuclear factor- (NF-) kappaB in 
      LPS-PG-stimulated HGF-1 cells. Furthermore, LPS-PG-induced phosphorylation of 
      extracellular regulated kinase (ERK) and Akt was abolished by CGA treatment, 
      while c-Jun N-terminal kinase (JNK) and p38 did not have any effect. 
      Consequently, these results suggest that CGA ameliorates LPS-PG-induced 
      inflammatory responses by attenuating TLR4/MyD88-mediated NF-kappaB, 
      phosphoinositide-3-kinase (PI3K)/Akt, and MAPK signaling pathways in HGF-1 cells.
CI  - Copyright (c) 2022 Chung Mu Park and Hyun-Seo Yoon.
FAU - Park, Chung Mu
AU  - Park CM
AUID- ORCID: 0000-0001-8477-6276
AD  - Department of Clinical Laboratory Science, Dong-Eui University, Republic of 
      Korea.
AD  - The Research Institute for Functional Health Materials, Dong-Eui University, 
      Republic of Korea.
FAU - Yoon, Hyun-Seo
AU  - Yoon HS
AUID- ORCID: 0000-0002-7455-5506
AD  - The Research Institute for Functional Health Materials, Dong-Eui University, 
      Republic of Korea.
AD  - Department of Dental Hygiene, Dong-Eui University, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20220409
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - 0 (Prostaglandins E)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 318ADP12RI (Chlorogenic Acid)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Chlorogenic Acid/metabolism/pharmacology
MH  - Cyclooxygenase 2/metabolism
MH  - Fibroblasts/metabolism
MH  - Humans
MH  - Inflammation/chemically induced/metabolism
MH  - Inflammation Mediators/metabolism
MH  - *Lipopolysaccharides/metabolism/pharmacology
MH  - Myeloid Differentiation Factor 88/metabolism
MH  - *NF-kappa B/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Prostaglandins E/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Toll-Like Receptor 4/metabolism
PMC - PMC9013303
COIS- The authors confirm that they have no conflict of interest.
EDAT- 2022/04/20 06:00
MHDA- 2022/04/21 06:00
PMCR- 2022/04/09
CRDT- 2022/04/19 06:00
PHST- 2021/09/08 00:00 [received]
PHST- 2022/03/11 00:00 [revised]
PHST- 2022/03/15 00:00 [accepted]
PHST- 2022/04/19 06:00 [entrez]
PHST- 2022/04/20 06:00 [pubmed]
PHST- 2022/04/21 06:00 [medline]
PHST- 2022/04/09 00:00 [pmc-release]
AID - 10.1155/2022/2127642 [doi]
PST - epublish
SO  - Mediators Inflamm. 2022 Apr 9;2022:2127642. doi: 10.1155/2022/2127642. 
      eCollection 2022.