Stomatin‐like protein‐2 relieve myocardial ischemia/reperfusion injury by adenosine 5′‐monophosphate‐activated protein kinase signal pathway

Previous studies have shown that stomatin‐like protein‐2 (SLP‐2) could regulate mitochondrial biogenesis and function. The study was designed to explore the contribution of SLP‐2 to the myocardial ischemia and reperfusion (I/R) injury. Anesthetized rats were treated with SLP‐2 and subjected to ischemia for 30 minutes before 3 hours of reperfusion. An oxygen‐glucose deprivation/reoxygenation model of I/R was established in H9C2 cells. In vivo, SLP‐2 significantly improved cardiac function recovery of myocardial I/R injury rats by increasing fractional shortening and ejection fraction. SLP‐2 pretreatment alleviated infarct area and myocardial apoptosis, which was paralleled by decreasing the level of cleaved caspase‐3 and the ratio of Bax/Bcl‐2, increasing the content of superoxide dismutase and reducing oxidative stress damage in serum. In addition, SLP‐2 increased the level of ATP and stabilized mitochondrial potential (Ψm). The present in vitro study revealed that overexpression with SLP‐2 reduced H9C2 cells apoptosis, accompanied by an increased level of ATP, the ratio of mitochondrial DNA/nuclear DNA, activities of complex II and V, and decreased the production of mitochondrial reactive oxygen species. Simultaneously, SLP‐2 activated the adenosine 5′‐monophosphate‐activated protein kinase (AMPK) signaling pathway in myocardial I/R injury rats and H9C2 cells. This study revealed that SLP‐2 mediates the cardioprotective effect against I/R injury by regulating AMPK signaling pathway. 1. Stomatin‐like protein‐2 (SLP‐2) mediates the cardioprotective effect against ischemia/reperfusion injury. 2. SLP‐2 treatment alleviated myocardial apoptosis and mitochondrial damage in rats and H9C2 cells.