TGFβ1 protects myocardium from apoptosis and oxidative damage after ischemia reperfusion

Myocardial apoptosis is an important pathologic basis of ischemia-reperfusion injury (I/R). Transforming growth factor β1 (TGFβ1) participates in the regulation of oxidative damage and apoptosis. TGFβ1 is upregulated in the repair process of I/R injury. It is speculated that TGFβ1 over-expression is involved in the endogenous protective mechanism of I/R injury. This study explores the significance of TGFβ1 in myocardial cell apoptosis after I/R.

Rat myocardial I/R injury model was established. Left ventricular ejection fraction (LVEF) and Left ventricular fractional shortening (LVFS) were detected by ultrasonic cardiogram. TGFβ1 expression in the myocardium was tested. H9C2 cells were cultured under ischemic hypoxic condition for 6 h, and then were treated by reoxygenation for 6 h to simulate I/R model. H9C2 cells were divided into three groups, including I/R+pIRES2-Blank, I/R+pIRES2 TGFβ1, and I/R+pIRES2-TGFβ1+LY364947. TGFβ1 mRNA and protein levels were evaluated. Cell apoptosis and reactive oxygen species (ROS) were determined by flow cytometry.

LVEF and LVFS significantly decreased in I/R group compared with Sham group. TGFβ1 mRNA and protein expressions in myocardium from I/R group up-regulated than the control. I/R treatment markedly elevated TGFβ1 mRNA and protein levels, increased ROS content, and enhanced cell apoptosis in H9C2 cells. Over-expression of TGFβ1 significantly weakened ROS production and apoptosis in H9C2 cells after I/R. TGFβ receptor inhibitor LY364947 restrained ROS production and apoptosis attenuation in H9C2 cells treated by TGFβ.

TGFβ1 alleviates myocardial cell apoptosis after I/R. Blocking TGFβ1 attenuates the protective effect of TGFβ1 on I/R injury.