Title: N-n-butyl haloperidol iodide protects cardiomyocytes against hypoxia/reoxygenation injury through an extracellular calcium-independent mechanism
Abstract: Objective To investigate the effect of N-n-butyl haloperidol iodide (F2 ) on hypoxia/reoxygenation (H/R) injury to cardiomyocytes cultured in extracellular-Ca2+-free medium and its mechanism. Methods The H/R models of neonatal rat cardiomyocytes in extracellular-Ca2+-free (Ca2+-free) medium were established. Changes in morphology and spontaneous beat of the cardiomyocytes were detected by inverted microscopy. Expressions of p-ERK1/2 and total ERK protein were examined by western-blot analyses. Results H/R caused damage to the cardiomycytes in Ca2+-free medium including cell shrinkage, pseudopod reduction and beat weakness. The expression level of p-ERK1/2, rather than that of total ERK, increased in the cardiomyocytes when subjected to H/R with Ca2+-free medium, indicating ERK1/2 became activated after H/R. Treatment with F2 during hypoxia and reoxygenation significantly attenuated the cardiomyocytes' injury in Ca2+-free medium and inhibited the overexpression of p-ERK but not the expression of total ERK. Conclusion F2 can protect cardiomyocytes against H/R-induced injury through a calcium-independent mechanism, which might be closely related to the inhibition effect of F2 on activation of ERK1/2 induced by Ca2+-free-H/R.
Publication Year: 2013
Publication Date: 2013-01-01
Language: en
Type: article
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