没食子酸丙酯对氧化型低密度脂蛋白诱导的内皮细胞损伤的保护作用。
Protective effect of propyl gallate against oxidized low-density lipoprotein-induced injury of endothelial cells.
作者信息
Ma Lu, Zhu Xiao-fa, Wu Yu-yun, Chen Ke-ji, Shi Da-zhuo, Yin Hui-jun
机构信息
Department of Geriatric Cardiology, the Navy General Hospital of Chinese PLA, Beijing, 100048, China,
出版信息
Chin J Integr Med. 2015 Apr;21(4):299-306. doi: 10.1007/s11655-014-1980-6. Epub 2015 Jan 14.
OBJECTIVE
To evaluate the protective effect of propyl gallate (PG), an alkyl ester of gallic acid which is an active ingredient of Radix Paeoniae, against oxidized low-density lipoprotein (ox-LDL)-induced apoptosis and death in endothelial cells (ECs) and to find out its preliminary mechanism.
METHODS
The cultured endothelial cells were divided into normal, model (ox-LDL), control (fetal bovine serum), PG high dose (20 μg/mL), PG middle dose (10 μg/mL), and PG low dose (5 μg/mL) groups, each derived from three different pools of umbilical cords. The model of injured human umbilical vein endothelial cells (HUVECs) was induced by ox-LDL. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, Hoechst 33258 staining, flow cytometry and measurement of nitrogen monoxidum (NO) release were used to evaluate the protective effect of PG against ox-LDL-induced apoptosis and death in HUVECs. To find out the mechanism of this protective effect, the expression of endothelial nitric oxide synthase (eNOS) mRNA, eNOS protein expression, immunofluorescence of intracellular reactive oxygen species (ROS) and activities of malondialdehyde (MDA), superoxidedismutase (SOD) and glutathione peroxidase (GPx) were observed.
RESULTS
PG significantly reduced ox-LDL-induced apoptosis and cell death. The percentage of cells death and apoptosis was significantly higher in the ox-LDL group than that in the control group (P<0.05). Compared with the control group, the cells death and apoptosis of PG group was no different (P>0.05). As compared with the ox-LDL group, results of the PG high dose group showed that cell viability was significantly increased (P<0.05), the level of NO release, expression of eNOS mRNA, densitometric value of eNOS protein expression, as well as the activities of SOD and GPx were all significantly higher (all P<0.05).
CONCLUSION
PG could potentially serve as a novel endothelial protective agent against ox-LDL-induced injury of endothelial cell.
目的
评估没食子酸丙酯（PG），一种没食子酸的烷基酯，芍药根的活性成分，对氧化低密度脂蛋白（ox-LDL）诱导的内皮细胞（ECs）凋亡和死亡的保护作用，并探究其初步机制。
方法
将培养的内皮细胞分为正常组、模型组（ox-LDL）、对照组（胎牛血清）、PG高剂量组（20μg/mL）、PG中剂量组（10μg/mL）和PG低剂量组（5μg/mL），每组均来源于三个不同的脐带样本库。用ox-LDL诱导人脐静脉内皮细胞（HUVECs）损伤模型。采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基-2H-四唑溴盐（MTT）法、Hoechst 33258染色、流式细胞术和一氧化氮（NO）释放量测定来评估PG对ox-LDL诱导的HUVECs凋亡和死亡的保护作用。为探究这种保护作用的机制，观察内皮型一氧化氮合酶（eNOS）mRNA的表达、eNOS蛋白表达、细胞内活性氧（ROS）的免疫荧光以及丙二醛（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）的活性。
结果
PG显著降低了ox-LDL诱导的凋亡和细胞死亡。ox-LDL组细胞死亡和凋亡的百分比显著高于对照组（P<0.05）。与对照组相比，PG组的细胞死亡和凋亡无差异（P>0.05）。与ox-LDL组相比，PG高剂量组的结果显示细胞活力显著增加（P<0.05），NO释放水平、eNOS mRNA表达、eNOS蛋白表达的光密度值以及SOD和GPx的活性均显著升高（均P<0.05）。
结论
PG可能作为一种新型的内皮保护剂，对抗ox-LDL诱导的内皮细胞损伤。
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