PMID- 30038553
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220318
IS  - 1559-3258 (Print)
IS  - 1559-3258 (Electronic)
IS  - 1559-3258 (Linking)
VI  - 16
IP  - 3
DP  - 2018 Jul-Sep
TI  - Tauroursodeoxycholic Acid Alleviates H(2)O(2)-Induced Oxidative Stress and 
      Apoptosis via Suppressing Endoplasmic Reticulum Stress in Neonatal Rat 
      Cardiomyocytes.
PG  - 1559325818782631
LID - 10.1177/1559325818782631 [doi]
LID - 1559325818782631
AB  - INTRODUCTION: We aimed to test the mechanism of protective effects of 
      tauroursodeoxycholic acid (TUDCA) on cardiovascular disease using cultured 
      cardiomyocytes. METHODS: Neonatal rat cardiomyocytes (NRCMs) were isolated and 
      cultured and then the cells were divided into 4 groups based on the treatments: 
      control group (cells treated with culture medium), H(2)O(2)/thapsigargin (TG) 
      group (cells treated with oxidative stress and endoplasmic reticulum [ER] stress 
      inducer), TUDCA group, and H(2)O(2)/TG + TUDCA group. The treated NRCMs were then 
      subjected to serial analyses including flow cytometry, enzyme-linked 
      immunosorbent assay, and Western blotting. RESULTS: Tauroursodeoxycholic acid 
      significantly attenuated H(2)O(2)-induced reactive oxygen species generation and 
      lactate dehydrogenase release and restored H(2)O(2)-induced reductions of 
      glutathione and superoxide dismutase levels in NRCMs. Tauroursodeoxycholic acid 
      also alleviated H(2)O(2)-induced cardiomyocytes apoptosis, as well as the 
      Bax/Bcl2 ratio compared with that of H(2)O(2) treated alone. In addition, TUDCA 
      suppressed TG-induced ER stress as reflected by inversing cell viability and the 
      expression levels of glucose-regulated protein 78 kDa and C/enhancer-binding 
      protein homologous protein. CONCLUSION: Our data indicated that TUDCA-mediated 
      inhibition on H(2)O(2)-induced oxidative stress and cardiomyocytes apoptosis was 
      through suppressing ER stress, and TUDCA possesses the potential to be developed 
      as therapeutic tool in clinical use for cardiovascular diseases.
FAU - Zhang, Lin
AU  - Zhang L
AUID- ORCID: 0000-0003-2153-1479
AD  - Department of Cardiology, Daqing Oilfield General Hospital, Daqing, Heilongjiang, 
      China.
FAU - Wang, Yanmin
AU  - Wang Y
AD  - Department of Circulatory Medicine, Daqing Longnan Hospital, Daqing, 
      Heilongjiang, China.
LA  - eng
PT  - Journal Article
DEP - 20180718
PL  - United States
TA  - Dose Response
JT  - Dose-response : a publication of International Hormesis Society
JID - 101308899
PMC - PMC6052504
OTO - NOTNLM
OT  - ER stress
OT  - H2O2-induced oxidative stress
OT  - cell apoptosis
OT  - neonatal mouse cardiomyocytes
OT  - tauroursodeoxycholic acid
COIS- Declaration of Conflicting Interests: The author(s) declared no potential 
      conflicts of interest with respect to the research, authorship, and/or 
      publication of this article.
EDAT- 2018/07/25 06:00
MHDA- 2018/07/25 06:01
PMCR- 2018/07/18
CRDT- 2018/07/25 06:00
PHST- 2017/10/24 00:00 [received]
PHST- 2018/03/28 00:00 [revised]
PHST- 2018/05/15 00:00 [accepted]
PHST- 2018/07/25 06:00 [entrez]
PHST- 2018/07/25 06:00 [pubmed]
PHST- 2018/07/25 06:01 [medline]
PHST- 2018/07/18 00:00 [pmc-release]
AID - 10.1177_1559325818782631 [pii]
AID - 10.1177/1559325818782631 [doi]
PST - epublish
SO  - Dose Response. 2018 Jul 18;16(3):1559325818782631. doi: 10.1177/1559325818782631. 
      eCollection 2018 Jul-Sep.