Abstract |
It has been previously reported that Rho‑kinase (ROCK) and poly ADP-ribose polymerase (PARP) serve critical roles in myocardial ischemia/reperfusion (I/R) injury. Studies have additionally demonstrated that the activation of ROCK and the expression of PARP are increased in I/R. However, the effect and mechanism of the two proteins remains to be fully elucidated in I/R. In addition, whether they can be influenced by each other is unclear. In the present study, it was demonstrated that ischemia followed by reperfusion resulted in a significant increase in ROCK and PARP. In addition, Y‑27632 (ROCK inhibitor) and 3‑aminobenzamide (3‑AB; PARP inhibitor) pretreatment rescued myocardial infarction size and cardiomyocyte apoptosis. The inhibitory role of Y‑27632 was observed to be superior to that of the 3‑AB group. In addition, Y‑27632 and 3‑AB diminished extracellular signal‑related kinase (ERK) phosphorylation and the production of tumor necrosis factor α and interleukin 6. Overall, the results of the present study suggested that the inhibition of ROCK leads to reduced myocardial infarction size and cardiomyocyte apoptosis via the PARP/ERK signaling pathway.
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Authors | Hongjun Bian, Yi Zhou, Bin Yu, Deya Shang, Fuli Liu, Bin Li, Jianni Qi |
Journal | Molecular medicine reports
(Mol Med Rep)
Vol. 16
Issue 2
Pg. 2002-2008
(Aug 2017)
ISSN: 1791-3004 [Electronic] Greece |
PMID | 28656263
(Publication Type: Journal Article)
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Chemical References |
- Poly(ADP-ribose) Polymerase Inhibitors
- Poly(ADP-ribose) Polymerases
- rho-Associated Kinases
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Topics |
- Animals
- Apoptosis
(drug effects)
- Cell Line
- Female
- Myocardial Reperfusion Injury
(enzymology, pathology)
- Myocytes, Cardiac
(drug effects, enzymology, pathology)
- Poly(ADP-ribose) Polymerase Inhibitors
(pharmacology)
- Poly(ADP-ribose) Polymerases
(metabolism)
- Rats, Wistar
- Signal Transduction
(drug effects)
- rho-Associated Kinases
(metabolism)
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