Scutellarin antagonizes ischemia-reperfusion injury to human cardiac microvascular endothelial cells by increasing ERK phosphorylation
10.16571/j.cnki.1008-8199.2017.09.004
- VernacularTitle:灯盏花乙素上调细胞外信号调节激酶表达拮抗人心脏微血管内皮细胞IR损伤
- Author:
Xian HUANG
;
Xiaoxue LI
;
Zhuo YU
;
Weimin YANG
;
Lin LI
- Keywords:
Scutellarin;
Ischemia-reperfusion injury;
Human cardiac microvascular endothelial cell;
Extracellular signal regulating kinase
- From:
Journal of Medical Postgraduates
2017;30(9):912-916
- CountryChina
- Language:Chinese
-
Abstract:
Objective Scutellarin (SCU), a Chinese traditional medicine, has a protective effect against ischemia-reperfusion (IR) induced myocardial injury, but it is not yet clear whether SCU acts against vascular endothelial IR injury via extracellular signal-regulated kinase 1/2 (ERK1/2).The aim of this study was to explore the effect of SCU on hypoxia-reoxygenation (HR)-induced injury to human cardiac microvascular endothelial cells (HCMECs) and its influence on the ERK1/2 signaling pathway.Methods HCMECs were subjected to normal culture and divided into a normal control, a DMSO, an SCU 1 μmol/L, and an SCU 10 μmol/L group.The model of HR injury was established by exposing the HCMECs to 12-h hypoxia and 12-h reoxygenation after treated with DMSO or SCU at 1 and 10 μmol/L for 2 hours.Then, the survival rate of the HCMECs was detected by MTT and trypan blue staining, the concentration of malondialdehyde (MDA) in the cells measured, and the expressions of the p-ERK1/2, ERK2 and GAPDH proteins determined by Western blot.Results SCU at 1 and 10 μmol/L significantly increased the survival rate of the normally cultured HCMECs ([110.40±2.34] and [122.00±1.25] ％) as compared with that of the normal control (100％) (P<0.05), while HR injury markedly decreased the vitality of the HCMECs ([68.00±4.06] ％) in comparison with that of the blank control (100％) (P<0.05).The survival rate of the HCMECs was remarkably higher in the HR+SCU 1 μmol/L and HR+SCU 10 μmol/L groups than in the HR model group ([90.53±3.67] and [92.04±2.32] ％) (P<0.05), and so was their vitality in the SCU 10 μmol/L group than in the normal control ([96.78±2.01] vs [90.06±1.85] ％, P<0.01), while their survival rate was significantly lower in the HR model than in the blank control ([73.72±4.91] vs [91.83±2.34] ％, P<0.01) and remarkably higher in the SCU 10 μmol/L ([87.59±2.64] ％) than in the HR model group (P<0.05).The MDA concentration in the HCMECs was markedly increased in the HR model and HR+DMSO groups as compared with the blank control (P<0.01), but decreased in the HR+SCU 1 μmol/L and HR+SCU 10 μmol/L groups in comparison with the HR model group (P<0.05).The expression of the p-ERK1/2 protein was significantly down-regulated in the HR model group as compared with the blank control (P<0.01), but up-regulated in the HR+SCU 10 μmol/L group in comparison with the HR model (P<0.01).Conclusion HR injury reduces the vitality of HCMECs, increases the MDA concentration, and down-regulates the expression of the p-ERK1/2 protein in HCMECs, while SCU acts against ischemia-reperfusion injury to HCMECs by increasing ERK phosphorylation.
