飞燕草素葡萄糖苷对抗高糖诱导的血管内皮细胞损伤的研究
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摘要
目的探讨飞燕草素葡萄糖苷(delphinidin-glucoside,DPg)是否可对抗高糖引起的血管内皮细胞氧化损伤,并阐明其可能的机制。方法血管内皮细胞在含或不含DPg(1、10、100μM)的高糖培养基中孵育后测定细胞生存率,同时用DCFH-DA法测定细胞活性氧生成,用底物法测定血红素氧化酶活性。结果 DPg可浓度依赖性地增加血管内皮细胞血红素氧化酶活性。血管内皮细胞暴露于高糖培养基后,细胞生存率明显下降,活性氧的生成增加;中、高浓度DPg(10、100μM)可抑制高糖诱导的细胞死亡,减少活性氧生成;血红素氧化酶抑制剂(ZnPPIX)可取消DPg的上述作用。结论DPg可能通过增加血红素加氧酶活性,抑制高糖诱导的ROS生成,从而减少血管内皮细胞死亡。
Objective To investigate whether delphinidin-glucoside(DPg) can protect against high glucose-induced oxidative stress in vascular endothelial cells, and to clarify its possible mechanism.Methods Vascular endothelial cells were cultured in high glucose medium with or without DPg(1, 10, or100 μM). Cell viability was measured using CCK-8 method. Reactive oxygen species(ROS) production was evaluated using DCFH-DA method. Heme oxygenase activity was determined by substrate method.Results DPg increased the heme oxygenase activity of endothelial cells in a concentration-dependent manner. After being exposed to high glucose medium, the survival rate of endothelial cells decreased and ROS production increased. Medium and high concentrations of DPg(10 or 100 μM) could inhibit high glucose-induced cell death and reduce ROS production, however ZnPPIX(a heme oxygenase inhibitor)prevented the protective effect of DPg. Conclusion DPg could reduce high glucose-induced ROS production and endothelial cell death by increase of heme oxygenase activity.
Objective To investigate whether delphinidin-glucoside(DPg) can protect against high glucose-induced oxidative stress in vascular endothelial cells, and to clarify its possible mechanism.Methods Vascular endothelial cells were cultured in high glucose medium with or without DPg(1, 10, or100 μM). Cell viability was measured using CCK-8 method. Reactive oxygen species(ROS) production was evaluated using DCFH-DA method. Heme oxygenase activity was determined by substrate method.Results DPg increased the heme oxygenase activity of endothelial cells in a concentration-dependent manner. After being exposed to high glucose medium, the survival rate of endothelial cells decreased and ROS production increased. Medium and high concentrations of DPg(10 or 100 μM) could inhibit high glucose-induced cell death and reduce ROS production, however ZnPPIX(a heme oxygenase inhibitor)prevented the protective effect of DPg. Conclusion DPg could reduce high glucose-induced ROS production and endothelial cell death by increase of heme oxygenase activity.
引文
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[2] CERIELLO A,MOTZ E. Is oxidative stress the pathogenic mechanism underlying insulin resistance,diabetes,and cardiovascular disease? The common soil hypothesis revisited[J]. Arterioscler Thromb Vasc Biol,2004,24(5):816-823.
[3] LI L,GUO C Y,JIA E Z,et al. Testosterone is negatively associated with the severity of coronary atherosclerosis in men[J]. Asian J Androl,2012,14(6):875-878.
[4] JIN X,CHEN M,YI L,et al. Delphinidin-3-glucoside protects human umbilical vein endothelial cells against oxidized lowdensity lipoprotein-induced injury by autophagy upregulation via the AMPK/SIRT1 signaling pathway[J]. Mol Nutr Food Res,2014,58(10):1941-1951.
[5] XIE X,ZHAO R,SHEN G X. Influence of delphinidin-3-glucoside on oxidized low-density lipoprotein-induced oxidative stress and apoptosis in cultured endothelial cells[J]. J Agric Food Chem,2012,60(7):1850-1856.
[6] OTTERBEIN L E,FORESTI R and MOTTERLINI R. Heme Oxygenase-1 and Carbon Monoxide in the Heart:The Balancing Act Between Danger Signaling and Pro-Survival[J]. Circ Res,2016,118(12):1940-1959.
[7] ISSAN Y,KORNOWSKI R,ARAVOT D,et al. Heme oxygenase-1 induction improves cardiac function following myocardial ischemia by reducing oxidative stress[J]. PLoS One,2014,9(3):e92246.
[8] QUAN S,KAMINSKI P M,YANG L,et al. Heme oxygenase-1 prevents superoxide anion-associated endothelial cell sloughing in diabetic rats[J]. Biochem Biophys Res Commun,2004,315(2):509-516.
[9] PERRELLA M A,YET S F. Role of heme oxygenase-1 in cardiovascular function[J]. Curr Pharm Des,2003,9(30):2479-2487.