PMID- 34738873
OWN - NLM
STAT- MEDLINE
DCOM- 20220216
LR  - 20240226
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 12
IP  - 2
DP  - 2021 Dec
TI  - p-Coumaric acid regulates macrophage polarization in myocardial 
      ischemia/reperfusion by promoting the expression of indoleamine 2, 3-dioxygenase.
PG  - 10971-10981
LID - 10.1080/21655979.2021.2001924 [doi]
AB  - Macrophage infiltration is a hallmark pathological change observed in early stage 
      myocardial ischemia/reperfusion (MI/R) injury and one of the main causes of 
      myocardial damage. Here, we investigated the effects of p-Coumaric acid (p-CA) on 
      macrophage polarization following MI/R injury and its mechanisms. In vitro, p-CA 
      decreases the expression of LPS/IFN-gamma-induced M1 macrophage markers (TNF-alpha, IL-6, 
      iNOS and CCL2) and increases IL-4-induced M2 macrophage markers (IL-10, CD206, 
      Arg1 and Mrc) in mouse bone marrow-derived macrophages (BMDMs). Additionally, 
      p-CA elevated indoleamine 2, 3-dioxygenase (IDO) protein expression levels, M2 
      macrophage polarization and M2 macrophage markers through IL-4. In contrast, 
      repression of IDO attenuated p-CA functions regulating BMDMs through IL-4. In 
      vivo, IDO expression was downregulated in mouse hearts subjected to MI/R injury. 
      Treatment of p-CA increased IDO expression in the hearts of MI/R mice. 
      Functionally, p-CA decreases M1 macrophage markers, the number of M1 macrophages 
      and inflammation around heart tissue following MI/R injury. Importantly, p-CA 
      reduces cardiomyocyte apoptosis caused by MI/R. Altogether, our study identified 
      that p-CA modulates macrophage polarization by promoting IDO expression and that 
      p-CA attenuates macrophage-mediated inflammation following MI/R by promoting M2 
      macrophage polarization through IDO.
FAU - Li, Na
AU  - Li N
AD  - Department of Cardiology, Beijing Key Laboratory of Hypertension, Beijing 
      Chaoyang Hospital, Capital Medical University, China.
FAU - Guo, Xueyuan
AU  - Guo X
AD  - Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, 
      Beijing Institute of Heart Lung and Blood Vessel Diseases.
FAU - Li, Rui
AU  - Li R
AD  - Department of Health Care, China-Japan Friendship Hospital, Beijing, China.
FAU - Zhou, Jian
AU  - Zhou J
AD  - Department of Cardiology, Beijing Key Laboratory of Hypertension, Beijing 
      Chaoyang Hospital, Capital Medical University, China.
FAU - Yu, Fangfang
AU  - Yu F
AD  - Department of Radiology, Beijing Chaoyang Hospital, Capital Medical University.
FAU - Yan, Xianliang
AU  - Yan X
AD  - Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, 
      Beijing Institute of Heart Lung and Blood Vessel Diseases.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Cardiotonic Agents)
RN  - 0 (Coumaric Acids)
RN  - 0 (Cytokines)
RN  - 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase)
RN  - 0 (Inflammation Mediators)
RN  - IBS9D1EU3J (p-coumaric acid)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Cardiotonic Agents/pharmacology
MH  - *Cell Polarity/drug effects
MH  - Coumaric Acids/*pharmacology
MH  - Cytokines/metabolism
MH  - Indoleamine-Pyrrole 2,3,-Dioxygenase/*metabolism
MH  - Inflammation Mediators/metabolism
MH  - Macrophages/drug effects/*enzymology/*pathology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Myocardial Reperfusion Injury/*enzymology/*pathology
MH  - Myocytes, Cardiac/drug effects/metabolism/pathology
MH  - Mice
PMC - PMC8810143
OTO - NOTNLM
OT  - IDO
OT  - P-coumaric acid
OT  - macrophage polarization
OT  - myocardial ischemia/reperfusion
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2021/11/06 06:00
MHDA- 2022/02/17 06:00
PMCR- 2021/11/29
CRDT- 2021/11/05 12:11
PHST- 2021/11/06 06:00 [pubmed]
PHST- 2022/02/17 06:00 [medline]
PHST- 2021/11/05 12:11 [entrez]
PHST- 2021/11/29 00:00 [pmc-release]
AID - 2001924 [pii]
AID - 10.1080/21655979.2021.2001924 [doi]
PST - ppublish
SO  - Bioengineered. 2021 Dec;12(2):10971-10981. doi: 10.1080/21655979.2021.2001924.