PMID- 35178131
OWN - NLM
STAT- MEDLINE
DCOM- 20220401
LR  - 20220401
IS  - 1875-8630 (Electronic)
IS  - 0278-0240 (Print)
IS  - 0278-0240 (Linking)
VI  - 2022
DP  - 2022
TI  - Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial 
      Arrhythmic Predisposition after Hypoxia.
PG  - 6517266
LID - 10.1155/2022/6517266 [doi]
LID - 6517266
AB  - Cardiomyocyte apoptosis, neural remodeling, and gap junction channel change play 
      critical roles in ventricular arrhythmia (VA) after acute myocardial infarction 
      (AMI). Urolithin B (UB), one of the gut metabolites of ellagitannins, a class of 
      antioxidant polyphenols, has various biological activities, but its direct role 
      in cardiomyocyte apoptosis, neural remodeling, and gap junction channel change 
      after AMI remains elusive. We investigated whether urolithin B reduced 
      susceptibility of myocardial arrhythmic after myocardial infarction (MI). In 
      vitro, the cardiomyocytes were subjected to hypoxia (94% N(2)/5% CO(2)/1% O(2)) 
      for 3 hours. Cardiomyocyte apoptosis was assessed by TUNEL staining and western 
      blotting. Urolithin B was found to decrease the number of apoptotic cells after 
      hypoxia. Moreover, there was a substantial decrease in the expression of neural 
      remodeling markers in the urolithin B treatment group. Urolithin B significantly 
      increased the expression level of gap junction channel protein. Mechanistically, 
      urolithin B inhibited cardiomyocyte apoptosis by activating Akt/the mammalian 
      target of rapamycin (mTOR) pathway, and the protection of urolithin B against 
      cardiomyocyte apoptosis was compromised with Akt gene silencing. Furthermore, 
      urolithin B suppressed nuclear translocation of nuclear factor-kB (NF-kappaB) to 
      facilitate nerve remodeling. Taken together, our findings suggested that UB 
      reduced the occurrence of myocardial arrhythmias after hypoxia via regulation of 
      the Akt/mTOR pathway and NF-kappaB nuclear translocation, which highlights the 
      potential of UB as a novel therapy for ischemic heart disease.
CI  - Copyright (c) 2022 Xin Huang et al.
FAU - Huang, Xin
AU  - Huang X
AD  - Department of Cardiology, The First Affiliated Hospital of Nanchang University, 
      Nanchang 330008, China.
AD  - Department of Cardiology, The First Hospital of Nanchang, The Third Affiliated 
      Hospital of Nanchang University, Affiliated Hospital of Sun Yat-sen University, 
      Nanchang 330008, China.
FAU - Gao, Hong
AU  - Gao H
AD  - Department of Cardiology, The First Hospital of Nanchang, The Third Affiliated 
      Hospital of Nanchang University, Affiliated Hospital of Sun Yat-sen University, 
      Nanchang 330008, China.
FAU - Jiang, Xiaojie
AU  - Jiang X
AD  - Department of Cardiology, The First Hospital of Nanchang, The Third Affiliated 
      Hospital of Nanchang University, Affiliated Hospital of Sun Yat-sen University, 
      Nanchang 330008, China.
FAU - Zheng, Zeqi
AU  - Zheng Z
AUID- ORCID: 0000-0002-0317-7851
AD  - Department of Cardiology, The First Affiliated Hospital of Nanchang University, 
      Nanchang 330008, China.
LA  - eng
PT  - Journal Article
DEP - 20220208
PL  - United States
TA  - Dis Markers
JT  - Disease markers
JID - 8604127
RN  - 0 (Coumarins)
RN  - 0 (urolithin B)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Arrhythmias, Cardiac/prevention & control
MH  - *Cell Hypoxia
MH  - Cells, Cultured
MH  - Coumarins/metabolism/*pharmacology
MH  - Disease Susceptibility
MH  - Gastrointestinal Microbiome/physiology
MH  - Mice
MH  - Myocytes, Cardiac/*drug effects
PMC - PMC8847032
COIS- The authors declare that there are no conflicts of interest regarding this study.
EDAT- 2022/02/19 06:00
MHDA- 2022/04/02 06:00
PMCR- 2022/02/08
CRDT- 2022/02/18 05:48
PHST- 2021/12/03 00:00 [received]
PHST- 2022/01/13 00:00 [revised]
PHST- 2022/01/20 00:00 [accepted]
PHST- 2022/02/18 05:48 [entrez]
PHST- 2022/02/19 06:00 [pubmed]
PHST- 2022/04/02 06:00 [medline]
PHST- 2022/02/08 00:00 [pmc-release]
AID - 10.1155/2022/6517266 [doi]
PST - epublish
SO  - Dis Markers. 2022 Feb 8;2022:6517266. doi: 10.1155/2022/6517266. eCollection 
      2022.