JAK2/STAT3信号通路介导灯盏花乙素抗人心脏微血管内皮细胞缺氧-复氧损伤

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.

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

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.