PMID- 31916051
OWN - NLM
STAT- MEDLINE
DCOM- 20210208
LR  - 20210208
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 43
IP  - 2
DP  - 2020 Apr
TI  - Isofraxidin Alleviates Myocardial Infarction Through NLRP3 Inflammasome 
      Inhibition.
PG  - 712-721
LID - 10.1007/s10753-019-01158-z [doi]
AB  - Isofraxidin is a well-known coumarin compound refined from traditional Chinese 
      medicines. It has been previously demonstrated to play an anti-inflammatory role 
      in various inflammatory conditions. However, the effect of isofraxidin on 
      myocardial infarction (MI) remains uncovered. In this study, we aimed to 
      investigate the effect of isofraxidin on MI. MI mice was created and 
      triphenyltetrazolium chloride (TTC) staining as well as echocardiographic 
      evaluation were conducted to analyze the severity of MI. Oxygen-glucose 
      deprivation (OGD) was used for the mimics of ischemic stress in murine 
      cardiomyocytes, and Cell Counting Kit-8 (CCK-8), Annexin V, and lactate 
      dehydrogenase (LDH) release assays were conducted for cell viability. Western 
      blot was used for the detection of NOD-like receptor family, pyrin domain 
      containing 3 (NLRP3), and adapter protein apoptosis-associated speck-like protein 
      (ASC) in heart tissues and cardiomyocytes. Real-time polymerase chain reaction 
      (PCR) and enzyme-linked immunosorbent assay (ELISA) were applied for the 
      detection of proinflammatory cytokines. We found that isofraxidin alleviated the 
      severity of MI and produced a cardio-protective effect against OGD damage. 
      Isofraxidin also decreased the overall and local inflammatory reaction in MI. 
      Those effects were through the inhibition of the NLRP3 inflammasome. Taken 
      together, we initially reported the cardio-protective and alleviative effect of 
      isofraxidin on MI and uncovered its underlying mechanism related to the NLRP3 
      inflammasome inhibition.
FAU - Chen, Guofan
AU  - Chen G
AD  - Department of Cardiology, The Affiliated Hospital of Hangzhou Normal University, 
      126 Wenzhou Road, Hangzhou, Zhejiang, China.
FAU - Song, Xiaozheng
AU  - Song X
AD  - Department of Cardiology, Shengli Oilfield Central Hospital, 31 Jinan Road, 
      Dongying, Shandong, China.
FAU - Lin, Dongming
AU  - Lin D
AD  - Department of Cardiology, The Second Affiliated Hospital of Zhejiang Chinese 
      Medical University, 318 Chaowang Road, Hangzhou, Zhejiang, China.
FAU - Xu, Peng
AU  - Xu P
AUID- ORCID: 0000-0002-9202-7985
AD  - Department of Cardiology, Affiliated Hangzhou First People's Hospital, Zhejiang 
      University School of Medicine, 261 Huansha Road, Hangzhou, Zhejiang, China. 
      hzxupeng1@126.com.
LA  - eng
GR  - 2018ZB057/Zhejiang Provincial Medicine Health Science and Technology Program/
PT  - Journal Article
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Coumarins)
RN  - 0 (Inflammasomes)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Nlrp3 protein, mouse)
RN  - 304915F056 (isofraxidin)
SB  - IM
MH  - Animals
MH  - Cell Survival/drug effects/physiology
MH  - Cells, Cultured
MH  - Coumarins/pharmacology/*therapeutic use
MH  - Inflammasomes/*antagonists & inhibitors/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myocardial Infarction/*drug therapy/metabolism/pathology
MH  - Myocytes, Cardiac/*drug effects/metabolism/pathology
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/*antagonists & 
      inhibitors/metabolism
OTO - NOTNLM
OT  - NLRP3 inflammasome
OT  - cardiomyocyte
OT  - inflammation
OT  - isofraxidin
OT  - myocardial infarction
EDAT- 2020/01/10 06:00
MHDA- 2021/02/09 06:00
CRDT- 2020/01/10 06:00
PHST- 2020/01/10 06:00 [pubmed]
PHST- 2021/02/09 06:00 [medline]
PHST- 2020/01/10 06:00 [entrez]
AID - 10.1007/s10753-019-01158-z [pii]
AID - 10.1007/s10753-019-01158-z [doi]
PST - ppublish
SO  - Inflammation. 2020 Apr;43(2):712-721. doi: 10.1007/s10753-019-01158-z.