Effect of propofol on calcium homeostasis in hypoxia-reoxygenated neonatal rat cardiomyocytes

Hyun Soo Kim, Woo Chul Chang, Ki Chul Hwang, In Geol Choi, Wyun Kon Park

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)


Intracellular Ca2+ overload induced by hypoxia-reoxygenation alters Ca2+ homeostasis, which plays an important role in myocardial cell injury. Even though propofol is known as a radical scavenger with Ca2+ channel blocking properties, little is known about cardioprotective effect associated with Ca2+ homeostasis in cardiomyocytes. In the present study, we showed that propofol protects cardiomyocytes against hypoxia-reoxygenation injury. In propofol-treated cardiomyocytes, we observed a decrease in the expression of pro-apoptotic protein Bax, cytochrome c, caspase-3 activation and intracellular Ca2+ content. We also found that propofol treatment enhanced expression of anti-apoptotic protein Bcl-2 and activation of ERK concerned with survival. Propofol attenuated alterations of genes involving Ca2+-regulatory mechanism and significantly modulated abnormal changes of SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. These results suggest that propofol modulates the expression of genes involved in Ca2+ homeostasis, thereby producing cardioprotective effects through a reduction in apoptotic cell death.

Original languageEnglish
Pages (from-to)139-145
Number of pages7
JournalEuropean Journal of Pharmacology
Issue number1-3
Publication statusPublished - 2008 Oct 10


  • Ca homeostasis
  • Cardiomyocytes
  • Hypoxia-reoxygenation
  • Propofol

ASJC Scopus subject areas

  • Pharmacology


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