PMID- 34194542
OWN - NLM
STAT- MEDLINE
DCOM- 20210721
LR  - 20220424
IS  - 1755-5922 (Electronic)
IS  - 1755-5914 (Print)
IS  - 1755-5914 (Linking)
VI  - 2021
DP  - 2021
TI  - Sodium Lactate Accelerates M2 Macrophage Polarization and Improves Cardiac 
      Function after Myocardial Infarction in Mice.
PG  - 5530541
LID - 10.1155/2021/5530541 [doi]
LID - 5530541
AB  - BACKGROUND: After myocardial infarction, anti-inflammatory macrophages perform 
      key homeostatic functions that facilitate cardiac recovery and remodeling. 
      Several studies have shown that lactate may serve as a modifier that influences 
      phenotype of macrophage. However, the therapeutic role of sodium lactate in 
      myocardial infarction (MI) is unclear. METHODS: MI was established by permanent 
      ligation of the left anterior descending coronary artery followed by injection of 
      saline or sodium lactate. Cardiac function was assessed by echocardiography. The 
      cardiac fibrosis area was assessed by Masson trichrome staining. Macrophage 
      phenotype was detected via qPCR, flow cytometry, and immunofluorescence. 
      Signaling proteins were measured by Western blotting. RESULTS: Sodium lactate 
      treatment following MI improved cardiac performance, enhanced anti-inflammatory 
      macrophage proportion, reduced cardiac myocytes apoptosis, and increased 
      neovascularization. Flow-cytometric analysis results reported that sodium lactate 
      repressed the number of the IL-6+, IL-12+, and TNF-alpha+ macrophages among 
      LPS-stimulated bone marrow-derived macrophages (BMDMs) and increased the mRNA 
      levels of Arg-1, YM1, TGF-beta, and IL-10. Mechanistic studies revealed that sodium 
      lactate enhanced the expression of P-STAT3. Furthermore, a STAT3 inhibitor 
      eliminated sodium lactate-mediated promotion macrophage polarization. CONCLUSION: 
      Sodium lactate facilitates anti-inflammatory M2 macrophage polarization and 
      protects against MI by regulating P-STAT3.
CI  - Copyright (c) 2021 Jialiang Zhang et al.
FAU - Zhang, Jialiang
AU  - Zhang J
AUID- ORCID: 0000-0001-7737-0323
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Huang, Fangyang
AU  - Huang F
AUID- ORCID: 0000-0002-3049-2996
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Chen, Li
AU  - Chen L
AUID- ORCID: 0000-0003-3719-8965
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Li, Guoyong
AU  - Li G
AUID- ORCID: 0000-0001-6260-2312
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Lei, Wenhua
AU  - Lei W
AUID- ORCID: 0000-0002-5324-3503
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Zhao, Jiahao
AU  - Zhao J
AUID- ORCID: 0000-0002-8153-8763
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Liao, Yanbiao
AU  - Liao Y
AUID- ORCID: 0000-0002-9771-6245
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Li, Yijian
AU  - Li Y
AUID- ORCID: 0000-0001-7660-3324
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Li, Changming
AU  - Li C
AUID- ORCID: 0000-0003-0416-6975
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
FAU - Chen, Mao
AU  - Chen M
AUID- ORCID: 0000-0002-5384-2813
AD  - Department of Cardiology, West China Hospital, Sichuan University, Chengdu, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20210605
PL  - England
TA  - Cardiovasc Ther
JT  - Cardiovascular therapeutics
JID - 101319630
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Inflammation Mediators)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - TU7HW0W0QT (Sodium Lactate)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Apoptosis/drug effects
MH  - Coronary Vessels/physiopathology
MH  - Disease Models, Animal
MH  - Echocardiography
MH  - Inflammation Mediators/metabolism
MH  - Macrophage Activation/*drug effects
MH  - Macrophages/*drug effects/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myocardial Infarction/*drug therapy/*physiopathology
MH  - Myocardium/metabolism
MH  - Myocytes, Cardiac/drug effects
MH  - STAT3 Transcription Factor/biosynthesis
MH  - Signal Transduction/drug effects
MH  - Sodium Lactate/*pharmacology
PMC - PMC8203388
COIS- The authors declare no conflicts of interest.
EDAT- 2021/07/02 06:00
MHDA- 2021/07/22 06:00
PMCR- 2021/06/05
CRDT- 2021/07/01 06:57
PHST- 2021/02/08 00:00 [received]
PHST- 2021/05/15 00:00 [revised]
PHST- 2021/05/25 00:00 [accepted]
PHST- 2021/07/01 06:57 [entrez]
PHST- 2021/07/02 06:00 [pubmed]
PHST- 2021/07/22 06:00 [medline]
PHST- 2021/06/05 00:00 [pmc-release]
AID - 10.1155/2021/5530541 [doi]
PST - epublish
SO  - Cardiovasc Ther. 2021 Jun 5;2021:5530541. doi: 10.1155/2021/5530541. eCollection 
      2021.