Lycopene protects against myocardial ischemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening.
Animals
Apoptosis
/ drug effects
Cell Survival
/ drug effects
Cells, Cultured
Lycopene
/ pharmacology
Mitochondria, Heart
/ drug effects
Mitochondrial Membrane Transport Proteins
/ drug effects
Mitochondrial Permeability Transition Pore
Myocardial Infarction
/ metabolism
Myocardial Reperfusion Injury
/ metabolism
Rats
apoptosis
lycopene
mitochondrial permeability transition pore
myocardial ischemia reperfusion injury
Journal
Drug design, development and therapy
ISSN: 1177-8881
Titre abrégé: Drug Des Devel Ther
Pays: New Zealand
ID NLM: 101475745
Informations de publication
Date de publication:
2019
2019
Historique:
received:
15
11
2018
accepted:
22
05
2019
entrez:
3
8
2019
pubmed:
3
8
2019
medline:
7
2
2020
Statut:
epublish
Résumé
Mitochondria permeability transition pore (MPTP) is an important therapeutic target for myocardial ischemia-reperfusion injury (MIRI). Lycopene (LP) is a potent antioxidant extracted from the mature fruits of plants and has been reported to protect against MIRI; however, its mechanism of action has yet to be completely elucidated. The present study aimed to investigate the role of MPTP in the cardioprotection of LP. H9c2 cells were pretreated with LP for 12 hrs and were subjected to 12-hr hypoxia/1-hr re-oxygenation, and cell viability was measured by a Cell Counting Kit-8 (CCK-8) assay. Male rats were subsequently intraperitoneally injected with LP for 5 consecutive days. At 24 hrs following the final injection, the rat hearts were isolated and subjected to 30-min ischemia/120-min reperfusion using Langendorff apparatus. The myocardial infarct size was measured by a TTC stain. Opening of the MPTP was induced by CaCl LP pretreatment significantly increased cell viability, reduced myocardial infarct size and decreased the apoptosis rate. In addition, opening and the decrease of ΔΨm were attenuated by LP and the expressions of cytochrome The results of the present study demonstrated that LP protects against MIRI by inhibiting MPTP opening, partly through the modulation of Bax and Bcl-2.
Sections du résumé
BACKGROUND
BACKGROUND
Mitochondria permeability transition pore (MPTP) is an important therapeutic target for myocardial ischemia-reperfusion injury (MIRI). Lycopene (LP) is a potent antioxidant extracted from the mature fruits of plants and has been reported to protect against MIRI; however, its mechanism of action has yet to be completely elucidated. The present study aimed to investigate the role of MPTP in the cardioprotection of LP.
METHODS
METHODS
H9c2 cells were pretreated with LP for 12 hrs and were subjected to 12-hr hypoxia/1-hr re-oxygenation, and cell viability was measured by a Cell Counting Kit-8 (CCK-8) assay. Male rats were subsequently intraperitoneally injected with LP for 5 consecutive days. At 24 hrs following the final injection, the rat hearts were isolated and subjected to 30-min ischemia/120-min reperfusion using Langendorff apparatus. The myocardial infarct size was measured by a TTC stain. Opening of the MPTP was induced by CaCl
RESULTS
RESULTS
LP pretreatment significantly increased cell viability, reduced myocardial infarct size and decreased the apoptosis rate. In addition, opening and the decrease of ΔΨm were attenuated by LP and the expressions of cytochrome
CONCLUSION
CONCLUSIONS
The results of the present study demonstrated that LP protects against MIRI by inhibiting MPTP opening, partly through the modulation of Bax and Bcl-2.
Identifiants
pubmed: 31371925
doi: 10.2147/DDDT.S194753
pii: 194753
pmc: PMC6635826
doi:
Substances chimiques
Mitochondrial Membrane Transport Proteins
0
Mitochondrial Permeability Transition Pore
0
Lycopene
SB0N2N0WV6
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2331-2342Déclaration de conflit d'intérêts
The authors report no conflicts of interest in this work.
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