Scutellarin protect human cardiac microvascular endothelial cells by hypoxia-reoxygenation injury involved JAK2/STAT3 signal pathway

Abstract Objective To investigate the antagonistic cell injury effect and molecular mechanism of scutellarin (SCU) in hypoxia reoxygenation (HR) treated human cardiac microvascular endothelial cells (HCMECs). Methods The method of 12 h hypoxia following by 12 h reoxygenation was used to culture HCMECs in vitro to built cell injury model. The groups were divided into control group, model (HR) group, and HR + SCU (0.1 µmol/L, 1 µmol/L, and 10 µmol/L) group. The cell viability was determined by MTT, and oxidative stress was detected by malondialdehyde (MDA) levels by biochemical assay kit. Protein expression of JAK2/p-JAK2 and STAT3/p-STAT3 were evaluated by Western blot. Results The results of MTT and MDA showed that HR decreased the cell viability ( P P P P Conclusion SCU took a protective effect on HR-treated HCMECs, and the molecular mechanism may be associated with the inhibition of JAK2/STAT3 signal transduction pathway.