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

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.