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.
This work was funded by the National Natural Science Foundation of China (Grant No.30960450, No.81560589, and No.81173110); Natrural Science Foundation of Yunnan Province Science and Technology Department and Education Department (Grant No.2017FE467 (-019), No.2018JS161, No.2014FA010, No. ZD2015009); Yunnan-USA joint research center of molecular medicines (2015ID001). We thank Mr. Renwei Zhang for the gift of SCU compound. We also thank Byron J. Aguilar for editing the manuscript.
