PMID- 32009962
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 10
DP  - 2019
TI  - Gaudichaudione H Inhibits Inflammatory Responses in Macrophages and Dextran 
      Sodium Sulfate-Induced Colitis in Mice.
PG  - 1561
LID - 10.3389/fphar.2019.01561 [doi]
LID - 1561
AB  - Macrophages-involved inflammation is considered to induce the damage in various 
      diseases. Herein, novel therapeutics inhibiting over-activation of macrophages 
      could prove an effective strategy to prevent inflammation-related diseases. 
      Gaudichaudione H (GH), which is a natural small molecular compound isolated from 
      Garcinia oligantha Merr. (Clusiaceae) has previously been demonstrated its 
      anti-cancer effects on several cancer cell lines. However, no report has been 
      published about the anti-inflammatory effect of GH to date. This study aims to 
      examine the anti-inflammatory effects and potential molecular mechanism of GH, 
      and provide new insights toward the treatment of inflammation. GH inhibited 
      nitric oxide (NO) production, inducible nitric oxide synthase (iNOS) and 
      cyclooxygenase-2 (COX-2) expression, cytokine interleukin-6 (IL-6) and tumor 
      necrosis factor-alpha (TNF-alpha) production, and messenger RNA (mRNA) expression to 
      attenuate inflammatory responses in lipopolysaccharide (LPS)-induced RAW 264.7 
      cells or stimulated bone marrow-derived macrophages (BMDMs). GH inhibited nuclear 
      factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) pathways, the 
      nuclear translocation of transcription factors NF-kappaB and activator protein 1 
      (AP-1), as well as upstream signaling of the toll-like receptor 4 (TLR4)-myeloid 
      differentiation primary response 88 (MyD88) pathway in stimulated macrophages. 
      Furthermore, the result of the intracellular signaling array showed that the 
      phosphorylation of adenosine 5'-monophosphate-activated protein kinase-alpha (AMPKalpha), 
      proline-rich Akt substrate of 40 kDa (PRAS40), and p38 could be down regulated by 
      GH in BMDMs, indicating that the mechanism by which GH inhibited inflammation may 
      be also associated with the energy metabolism pathway, PRAS40-mediated NF-kappaB 
      pathway, cell proliferation, apoptosis, and autophagy, etc. In addition, GH 
      alleviated dextran sodium sulfate (DSS)-induced colitis in mice by ameliorating 
      weight loss, stool consistency change, blood in the stool, and colon shortening. 
      GH decreased the protein and mRNA levels of IL-6 and TNF-alpha, iNOS and COX-2 mRNA 
      expression, the activation of NF-kappaB and MAPK pathways, the phosphorylation of 
      AMPKalpha and PRAS40, histological damage, and infiltration of macrophages in the 
      colons of mice with DSS-induced colitis. Taken together, our results support that 
      GH exerts the anti-inflammatory effects in macrophages in vitro through 
      regulation of NF-kappaB and MAPK pathways, and DSS-induced colitis mouse model in 
      vivo. These findings suggest that GH may be a promising candidate in treating 
      macrophage-related inflammatory disease.
CI  - Copyright (c) 2020 Jiang, Xiao, Fu, Tang, Lertnimitphun, Kim, Zheng, Tan, Lu and 
      Xu.
FAU - Jiang, Yiwen
AU  - Jiang Y
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Xiao, Lianbo
AU  - Xiao L
AD  - Institute of Arthritis Research, Shanghai Academy of Chinese Medical Sciences, 
      Guanghua Integrative Medicine Hospital, Shanghai, China.
FAU - Fu, Wenwei
AU  - Fu W
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Tang, Yuexun
AU  - Tang Y
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Lertnimitphun, Peeraphong
AU  - Lertnimitphun P
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Kim, Nami
AU  - Kim N
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Zheng, Changwu
AU  - Zheng C
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Tan, Hongsheng
AU  - Tan H
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Lu, Yue
AU  - Lu Y
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
FAU - Xu, Hongxi
AU  - Xu H
AD  - School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 
      Shanghai, China.
LA  - eng
PT  - Journal Article
DEP - 20200117
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC6978770
OTO - NOTNLM
OT  - colitis
OT  - gaudichaudione H
OT  - macrophages
OT  - mitogen-activated protein kinases
OT  - nitric oxide
OT  - nuclear factor-kappaB
EDAT- 2020/02/06 06:00
MHDA- 2020/02/06 06:01
PMCR- 2020/01/17
CRDT- 2020/02/04 06:00
PHST- 2019/07/17 00:00 [received]
PHST- 2019/12/03 00:00 [accepted]
PHST- 2020/02/04 06:00 [entrez]
PHST- 2020/02/06 06:00 [pubmed]
PHST- 2020/02/06 06:01 [medline]
PHST- 2020/01/17 00:00 [pmc-release]
AID - 10.3389/fphar.2019.01561 [doi]
PST - epublish
SO  - Front Pharmacol. 2020 Jan 17;10:1561. doi: 10.3389/fphar.2019.01561. eCollection 
      2019.