Abstract
This study was designed to investigate whether Resveratrol (Res) could be a prophylactic factor in the prevention of I/R injury and to shed light on its underlying mechanism. Primary culture of neonatal rat cardiomyocytes were randomly distributed into three groups: the normal group (cultured cardiomyocytes were in normal conditions), the I/R group (cultured cardiomyocytes were subjected to 2 h simulated ischemia followed by 4 h reperfusion), and the Res+I/R group (100 µmol/L Res was administered before cardiomyocytes were subjected to 2 h simulated ischemia followed by 4 h reperfusion). To test the extent of cardiomyocyte injury, several indices were detected including cell viability, LDH activity, Na+-K+-ATPase and Ca2+-ATPase activity. To test apoptotic cell death, caspase-3 activity and the expression of Bcl-2/Bax were detected. To explore the underlying mechanism, several inhibitors, intracellular calcium, SOD activity and MDA content were used to identify some key molecules involved. Res increased cell viability, Na+-K+-ATPase and Ca2+-ATPase activity, Bcl-2 expression, and SOD level. While LDH activity, capase-3 activity, Bax expression, intracellular calcium and MDA content were decreased by Res. And the effect of Res was blocked completely by either L-NAME (an eNOS inhibitor) or MB (a cGMP inhibitor), and partly by either DS (a PKC inhibitor) or Glybenclamide (a KATP inhibitor). Our results suggest that Res attenuates I/R injury in cardiomyocytes by preventing cell apoptosis, decreasing LDH release and increasing ATPase activity. NO, cGMP, PKC and KATP may play an important role in the protective role of Res. Moreover, Res enhances the capacity of anti-oxygen free radical and alleviates intracellular calcium overload in cardiomyocytes.
Highlights
Acute myocardial infarction (AMI) is the most common type of cardiovascular diseases with a high mortality and morbidity nowadays
Effect of Res on cell viability By using trypan blue transmission method, the blue-stained cells in the ischemia/ reperfusion (I/R) group increased and it was of significance compared with the normal group
The activity of Na+-K+-ATPase and Ca2+-ATPase in the I/R group was significantly lower than the normal group, which indicated that I/ R attenuated Na+-K+-ATPase and Ca2+-ATPase function
Summary
Acute myocardial infarction (AMI) is the most common type of cardiovascular diseases with a high mortality and morbidity nowadays. AMI leads to the death of a great many of cardiomyocytes. The treatment has been improved a lot, the recovery of patients is still unsatisfactory. One of the most important factors responsible for the poor recovery is ischemia/ reperfusion (I/R) injury occurring during the treatment [1], which leads more cardiomyocytes to death and weakens the effect of reperfusion therapy. I/R injury is a complicated process which involves various mechanisms. As one of the most important mechanisms involved in I/R injury, plays an important role in the initiation and progression of I/R injury [2]. Kajstura et al [3] showed that apoptosis was the predominant mode of cardiomyocyte death induced by I/R. There are some other factors [4], such as calcium overload, and reactive oxygen species (ROS) generation, contributing to cell death during I/R injury
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