The cardioprotective effect and mechanism of bioactive glass on myocardial reperfusion injury.

Myocardial reperfusion treatment for ischemic infarction may cause lethal injury of cardiomyocytes, which is known as ischemia/reperfusion (I/R) injury. As a kind of prospective biomaterial with superior properties, the application of bioactive glasses (BGs) in myocardial tissue engineering have received great interests. In this study, the cardioprotective effect and relevant mechanism of BG on myocardial reperfusion injury were investigated. H9c2 cardiomyocytes were pretreated with BG extracts and then cultured in hypoxic environment for 30 min followed by reoxygenation for 1 h. The activity of released lactate dehydrogenase (LDH) and the content of malondialdehyde (MDA) in H9c2 cells were tested by assay kits. Cell viability was analyzed by Live/Dead staining assay and the number of living cells was detected by Cell Counting Kit-8 (CCK-8) assay. The cytoskeletal protein F-actin was stained and observed under inverted fluorescence microscope. Mitochondrial membrane potential (MMP) level, reactive oxygen species (ROS) production and apoptosis ratio were evaluated by fluorescent observation and flow cytometry simultaneously. The gene expressions relevant to apoptosis were detected by quantitative real time polymerase chain reaction (qRT-PCR) analysis. The results showed that BG extracts effectively inhibited hypoxia/reoxygenation (H/R)-induced cell injury by suppressing oxidative stress and mitochondrial permeability transition (MPT) within H9c2 cells. Meanwhile, apoptosis caused by H/R injury was alleviated and three classic apoptotic signaling pathways were proved to be regulated by BG extracts. Further analysis showed that phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway was up-regulated in H/R-induced H9c2 cells by BG extracts, leading to relieved cellular apoptosis. These results indicated that BG might exert cardioprotective effect in reperfusion injury when applied in myocardial tissue regeneration and repair.