PMID- 35898278
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220729
IS  - 2297-055X (Print)
IS  - 2297-055X (Electronic)
IS  - 2297-055X (Linking)
VI  - 9
DP  - 2022
TI  - Sinapic Acid Attenuated Cardiac Remodeling After Myocardial Infarction by 
      Promoting Macrophage M2 Polarization Through the PPARgamma Pathway.
PG  - 915903
LID - 10.3389/fcvm.2022.915903 [doi]
LID - 915903
AB  - BACKGROUND: Macrophage polarization is an important regulatory mechanism of 
      ventricular remodeling. Studies have shown that sinapic acid (SA) exerts an 
      anti-inflammatory effect. However, the effect of SA on macrophages is still 
      unclear. OBJECTIVES: The purpose of the study was to investigate the role of SA 
      in macrophage polarization and ventricular remodeling after myocardial infarction 
      (MI). METHODS: An MI model was established by ligating the left coronary artery. 
      The rats with MI were treated with SA for 1 or 4 weeks after MI. The effect of SA 
      on bone marrow-derived macrophages (BMDMs) was also observed in vitro. RESULTS: 
      Cardiac systolic dysfunction was significantly improved after SA treatment. SA 
      reduced MCP-1 and CCR2 expression and macrophage infiltration. SA decreased the 
      levels of the inflammatory factors TNF-alpha, IL-1alpha, IL-1beta, and iNOS and increased 
      the levels of the M2 macrophage markers CD206, Arg-1, IL-10, Ym-1, Fizz-1, and 
      TGF-beta at 1 week after MI. SA significantly increased CD68(+)/CD206(+) macrophage 
      infiltration. Myocardial interstitial fibrosis and MMP-2 and MMP-9 levels were 
      decreased, and the sympathetic nerve marker TH and nerve sprouting marker GAP43 
      were suppressed after SA treatment at 4 weeks after MI. The PPARgamma level was 
      notably upregulated after SA treatment. In vitro, SA also increased the 
      expression of PPARgamma mRNA in BMDMs and IL-4-treated BMDMs in a 
      concentration-dependent manner. SA enhanced Arg1 and IL-10 expression in BMDMs, 
      and the PPARgamma antagonist GW9662 attenuated M2 macrophage marker expression. 
      CONCLUSIONS: Our results demonstrated that SA attenuated structural and neural 
      remodeling by promoting macrophage M2 polarization via PPARgamma activation after MI.
CI  - Copyright (c) 2022 Yang, Xiong, Zou, Wang, Hu and Zhao.
FAU - Yang, Mei
AU  - Yang M
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
AD  - Cardiovascular Research Institute, Wuhan University, Wuhan, China.
AD  - Hubei Key Laboratory of Cardiology, Wuhan, China.
FAU - Xiong, Jun
AU  - Xiong J
AD  - Department of Emergency, Renmin Hospital of Wuhan University, Wuhan, China.
FAU - Zou, Qiang
AU  - Zou Q
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
AD  - Cardiovascular Research Institute, Wuhan University, Wuhan, China.
AD  - Hubei Key Laboratory of Cardiology, Wuhan, China.
FAU - Wang, Xi
AU  - Wang X
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
AD  - Cardiovascular Research Institute, Wuhan University, Wuhan, China.
AD  - Hubei Key Laboratory of Cardiology, Wuhan, China.
FAU - Hu, Ke
AU  - Hu K
AD  - Department of Respiratory and Critical Care Medicine, Renmin Hospital of Wuhan 
      University, Wuhan, China.
FAU - Zhao, Qingyan
AU  - Zhao Q
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
AD  - Cardiovascular Research Institute, Wuhan University, Wuhan, China.
AD  - Hubei Key Laboratory of Cardiology, Wuhan, China.
LA  - eng
PT  - Journal Article
DEP - 20220711
PL  - Switzerland
TA  - Front Cardiovasc Med
JT  - Frontiers in cardiovascular medicine
JID - 101653388
PMC - PMC9309384
OTO - NOTNLM
OT  - PPARgamma
OT  - interstitial fibrosis
OT  - macrophage
OT  - myocardial infarction
OT  - sinapic acid
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/07/29 06:00
MHDA- 2022/07/29 06:01
PMCR- 2022/01/01
CRDT- 2022/07/28 02:04
PHST- 2022/04/08 00:00 [received]
PHST- 2022/06/02 00:00 [accepted]
PHST- 2022/07/28 02:04 [entrez]
PHST- 2022/07/29 06:00 [pubmed]
PHST- 2022/07/29 06:01 [medline]
PHST- 2022/01/01 00:00 [pmc-release]
AID - 10.3389/fcvm.2022.915903 [doi]
PST - epublish
SO  - Front Cardiovasc Med. 2022 Jul 11;9:915903. doi: 10.3389/fcvm.2022.915903. 
      eCollection 2022.