中文摘要：

目的 灯盏花乙素（SCU）可拮抗心肌IR损伤,但SCU是否通过细胞外信号调节激酶（ERK1/2）通路拮抗IR所致血管内皮细胞损伤尚不清楚。文中探讨SCU在缺氧-复氧（HR）诱导的人心脏微血管内皮细胞（HCMEC）损伤中的作用及对ERK1/2信号通路的影响。方法 体外培养的HCMEC分别进行正常培养和缺氧12 h-复氧12 h建立IR模型（HR）处理。正常培养条件下,将HCMEC分为正常对照组、DMSO组、SCU 1μmol/L组和SCU 10μmol/L组。给予HCMEC IR损伤处理后,分为空白对照组、HR模型组、HR＋DMSO组、HR＋SCU 1μmol/L组和HR＋SCU 10μmol/L组。将HCMEC与SCU或DMSO预孵育2 h后行HR处理。采用MTT法和锥虫蓝染色检测细胞存活率,并检测HCMEC的丙二醛（MDA）浓度。Western blot检测p-ERK1/2、ERK2和GAPDH蛋白表达情况。结果 MTT检测结果显示,与正常对照组细胞存活率（100%）比较,SCU 1μmol/L组和SCU 10μmol/L组[（110.40±2.34）%和（122±1.25）%]均增加（P〈0.05）;与空白对照组细胞活力（100%）比较,HR模型组[（68.00±4.06）%]下降（P〈0.05）,与HR模型组细胞存活率比较,HR＋SCU 1μmol/L组和HR＋SCU 10μmol/L组[（90.53±3.67）%、（92.04±2.32）%]增加（P〈0.05）。锥虫蓝染色显示,与正常对照组细胞活力[（90.06±1.85）%]比较,SCU 10μmol/L组[（96.78±2.01）%]增加（P〈0.05）;与空白对照组[（91.83±2.34）%]比较,HR模型组细胞存活率[（73.72±4.91）%]下降（P〈0.01）,与HR模型组比较,HR＋SCU 10μmol/L组细胞存活率[（87.59±2.64）%]增加（P〈0.05）。与空白对照组比较,HR模型组、HR＋DMSO组MDA明显增加（P〈0.01）;与HR模型组比较,HR＋SCU 1μmol/L组和HR＋SCU 10μmol/L组MDA含量减少（P〈0.05）。与空白对照组比较,HR模型组p-ERK1/2蛋白表达明显降低（P〈0.01）;与HR模型组比较,HR＋SCU 10μmol/L组p-ERK1/2蛋白表达明显增加（P〈0.01）。结论 HR损伤导致HCMEC细胞活力下降、MDA增加和p-ERK1/2?

英文摘要：

Objective Scutellarin （SCU） , a Chinese tra-ditional 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 jjimol/L, and an SCU 10 jjimol/L group. The model of HR injury was established by exposing the HC-MECs to 12-h hypoxia and 12-h reoxygenation after treated with DMSO or SCU at 1 and 10 jjimol/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-ERKl/2, ERK2 and GAPDH proteins determined by Western blot. Results SCU at 1 and 10 jjimol/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 jjimol/L and HR＋SCU 10 jjimol/L groups than in the HR model group （ [90.53±3.67] and [92.04±2.32] ,and sowas their vitality in the SCU 10 jjimol/L group than in the normal control （ [96.78±2.01] 仍 [9 0 .06±1.85] % ,P〈0 .0 1 ） , wtdle their survival rate was significantly lower in the HR model than in the blank control （[ 73.72±4.91 ] 仍 [91.83±2.34] % , P〈0 .0 1） and re-markably higher in the SCU 10 jjimol/L （ [87.59±2.64] %） than in the HR model group （P〈0.0