N -n-butyl haloperidol iodide ameliorates cardiomyocytes hypoxia/reoxygenation injury by extracellular calcium-dependent and -independent mechanisms
Oxidative Medicine and Cellular Longevity, ISSN: 1942-0994, Vol: 2013, Page: 912310
2013
- 10Citations
- 8Captures
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Metrics Details
- Citations10
- Citation Indexes10
- 10
- CrossRef1
- Captures8
- Readers8
Article Description
N-n-butyl haloperidol iodide (F) has been shown to antagonize myocardial ischemia/reperfusion injury by blocking calcium channels. This study explores the biological functions of ERK pathway in cardiomyocytes hypoxia/reoxygenation injury and clarifies the mechanisms by which F ameliorates cardiomyocytes hypoxia/reoxygenation injury through the extracellular-calcium-dependent and -independent ERK1/2-related pathways. In extracellularcalcium-containing hypoxia/reoxygenation cardiomyocytes, PKC and ERK1/2 were activated, Egr-1 protein level and cTnI leakage increased, and cell viability decreased. The ERK1/2 inhibitors suppressed extracellular-calcium- containing-hypoxia/reoxygenation-induced Egr-1 overexpression and cardiomyocytes injury. PKC inhibitor downregulated extracellularcalcium-containing-hypoxia/ reoxygenation-induced increase in p-ERK1/2 and Egr-1 expression. F downregulated hypoxia/reoxygenation-induced elevation of p-PKC, p-ERK1/2, and Egr-1 expression and inhibited cardiomyocytes damage. The ERK1/2 and PKC activators antagonized F's effects. In extracellular-calcium-free- hypoxia/reoxygenation cardiomyocytes, ERK1/2 was activated, LDH and cTnI leakage increased, and cell viability decreased. F and ERK1/2 inhibitors antagonized extracellular-calcium-free-hypoxia/reoxygenation-induced ERK1/2 activation and suppressed cardiomyocytes damage. The ERK1/2 activator antagonized F's above effects. F had no effect on cardiomyocyte cAMP content or PKA and Egr-1 expression. Altogether, ERK activation in extracellular-calcium-containing and extracellular-calcium-free hypoxia/reoxygenation leads to cardiomyocytes damage. F may ameliorate cardiomyocytes hypoxia/reoxygenation injury by regulating the extracellular-calcium-dependent PKC/ERK1/2/Egr-1 pathway and through the extracellular-calcium-independent ERK1/2 activation independently of the cAMP/PKA pathway or Egr-1 overexpression. © 2013 Yanmei Zhang et al.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84890031730&origin=inward; http://dx.doi.org/10.1155/2013/912310; http://www.ncbi.nlm.nih.gov/pubmed/24392181; http://www.hindawi.com/journals/omcl/2013/912310/; https://dx.doi.org/10.1155/2013/912310; https://www.hindawi.com/journals/omcl/2013/912310/
Hindawi Limited
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