PMID- 36830962
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230228
IS  - 2227-9059 (Print)
IS  - 2227-9059 (Electronic)
IS  - 2227-9059 (Linking)
VI  - 11
IP  - 2
DP  - 2023 Feb 1
TI  - Melatonin Supplement Plus Exercise Effectively Counteracts the Challenges of 
      Isoproterenol-Induced Cardiac Injury in Rats.
LID - 10.3390/biomedicines11020428 [doi]
LID - 428
AB  - To explore the combined effects of exercise and melatonin supplement against the 
      challenges of isoproterenol-induced cardiac oxidative stress and injury in rats., 
      the expression of peroxisome proliferator-activated receptor gamma 
      co-activator-1alpha (PGC-1alpha), mitochondrial biogenesis, and adenosine triphosphate 
      (ATP) was up-regulated in cardiac muscle in normal rats and in a melatonin and 
      exercise regimented group. Cardiac injury was induced by two subcutaneous 
      injections of isoproterenol in the rats. The combination of exercise and 
      melatonin supplement successfully counteracted the isoproterenol-induced cardiac 
      injury, which is reflected by the improved hemodynamic parameters, reduction in 
      oxidative stress markers, and cardiac injury serum markers (cardiac troponin-I 
      and creatine kinase-MB). The cardiac tissue level of ATP, expression of PGC-1alpha 
      and mitochondrial biogenesis-related genes, mitochondrial membrane potential, and 
      the activities of typical antioxidants (glutathione, superoxide dismutase) were 
      preserved, whereas the levels of reactive oxygen species, lipid peroxidation, and 
      inflammatory cytokines were suppressed in the melatonin and exercise regimented 
      (MEI) group compared to the group treated with isoproterenol alone. Furthermore, 
      the expression of endoplasmic reticular stress- and apoptosis-related proteins 
      (Bax, Bcl2, and caspase-3) was also effectively suppressed in the MEI group. 
      Therefore, the present study suggests that melatonin supplement in combination 
      with exercise prevents cardiac injury, possibly through the preservation of 
      mitochondrial function and inhibition of oxidative stress in rats.
FAU - Rahman, Md Mahbubur
AU  - Rahman MM
AUID- ORCID: 0000-0002-0243-7746
AD  - Department of Veterinary Pharmacology and Toxicology, College of Veterinary 
      Medicine, Jeonbuk National University, Iksan 54596, Republic of Korea.
AD  - Department of Physiology, College of Medicine, Gachon University, Incheon 21999, 
      Republic of Korea.
FAU - Yang, Dong Kwon
AU  - Yang DK
AUID- ORCID: 0000-0002-7674-3690
AD  - Department of Veterinary Pharmacology and Toxicology, College of Veterinary 
      Medicine, Jeonbuk National University, Iksan 54596, Republic of Korea.
LA  - eng
GR  - NRF- 2021R1I1A1A01054531/The Ministry of Science and Technology/
GR  - NRF-2021R1A5A2030333/National Research Foundation (NRF) of Republic of Korea/
PT  - Journal Article
DEP - 20230201
PL  - Switzerland
TA  - Biomedicines
JT  - Biomedicines
JID - 101691304
PMC - PMC9953439
OTO - NOTNLM
OT  - antioxidant
OT  - cardiac injury
OT  - exercise
OT  - isoproterenol
OT  - melatonin
OT  - oxidative stress
COIS- The authors declare no conflict of interest.
EDAT- 2023/02/26 06:00
MHDA- 2023/02/26 06:01
PMCR- 2023/02/01
CRDT- 2023/02/25 01:27
PHST- 2022/11/23 00:00 [received]
PHST- 2023/01/18 00:00 [revised]
PHST- 2023/01/24 00:00 [accepted]
PHST- 2023/02/25 01:27 [entrez]
PHST- 2023/02/26 06:00 [pubmed]
PHST- 2023/02/26 06:01 [medline]
PHST- 2023/02/01 00:00 [pmc-release]
AID - biomedicines11020428 [pii]
AID - biomedicines-11-00428 [pii]
AID - 10.3390/biomedicines11020428 [doi]
PST - epublish
SO  - Biomedicines. 2023 Feb 1;11(2):428. doi: 10.3390/biomedicines11020428.