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 < 0.05) and increased MDA level significantly (P < 0.05), SCU played a contrary role in these processes. Western blot analysis indicates that, the expression of JAK2 and p-JAK2, STAT3, and p-STAT3 were increased in model group when compared with control group (P < 0.05); Compared with model group, their expression were reduced by SCU (P < 0.05). 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.