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牡蛎糖胺聚糖对H_2O_2所致血管内皮细胞氧化损伤的保护作用 被引量:4

PROTECTIVE EFFECTS OF OYSTER GLYCOSAMINOGLYCAN ON THE INJURY OF VASCULAR ENDOTHELIAL CELLS INDUCED BY HYDROGEN PEROXIDE
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摘要 目的了解牡蛎糖胺聚糖(O-GAG)对过氧化氢所致血管内皮细胞(VECs)氧化损伤的保护作用及其机制。方法采用人脐静脉内皮细胞株ECV304体外培养的方法,建立H2O2诱导的血管内皮细胞损伤模型,实验分为正常对照组、损伤模型组(过氧化氢50 mg/L)、肝素组(肝素200 mg/L,过氧化氢50 mg/L)、O-GAG保护组(O-GAG 10、50、100、200、400、800 mg/L,过氧化氢50 mg/L)、O-GAG对照组(O-GAG 100、200、400 mg/L)。采用噻唑蓝(MTT)比色法观察O-GAG对血管内皮细胞增殖活性的影响,黄嘌呤氧化酶法检测细胞超氧化物歧化酶(SOD)活性。结果与正常对照组相比,损伤模型组细胞的增殖活性和SOD的活活性均明显降低(F=137.23、135.40,q=5.26、5.34,P〈0.01),而O-GAG对照组(100、200 mg/L)的细胞增殖活性明显增高(q=3.40、3.81,P〈0.05)。与损伤模型组相比,O-GAG各保护组(50-800 mg/L)细胞增殖活性明显增加(q=3.40-5.23,P〈0.05、0.01),SOD活性明显升高(q=4.46-5.07,P〈0.01)。结论O-GAG对过氧化氢所致血管内皮细胞的氧化损伤具有保护作用,其作用机制可能与增加细胞内SOD活性有关。 Objective To assess the protective effect of oyster glycosaminoglycan (O-GAG) on the injury of vascular endothelial cells (VECs) induced by hydrogen peroxide and its corresponding mechanism. Methods The endothelial cell strain from human umbilical vein was cultured and a model of VECs injured by hydrogen peroxide (H2O2) was established. This study was conducted as follows: normal control group, O-GAG control group (O-GAG 100, 200, and 400 mg/L), H2O2-injury group (H2O2 50 rag/L), heparingroup(heparin 200 mg/L,H2O2 50 mg/L) and O-GAG protective group(O-GAG 10, 50, 100, 200, 400, and 800 mg/L, H2O2 50 mg/L). Influence of O-GAG on proliferate activity of VECs was tested by means of MTT assay and levels of SOD were tested by xanthine oxidase. Results Compared with the normal control group, the proliferate activity of VECs of OGAG control group was significantly increased (q= 3.40, P〈0. 05), while the proliferate activity of VECs and the levels of SOD of H2O2-injurygroup were markedly decreased (F=137. 23,135. 40;q=5. 26,5. 34;P〈0.01). Compared with (YGAG control group, the proliferate activity of VECs and levels of SOD of the O-GAG protective group were more significantly increased (q= 3.40-5.11 ;P〈0.05,0. 01). Conclusion O-GAG can protect the VECs from H2O2-induced injury, and the possible mechanism may refer to the increasing of SOD activity in the injured VECs.
出处 《青岛大学医学院学报》 CAS 2007年第3期262-264,共3页 Acta Academiae Medicinae Qingdao Universitatis
关键词 牡蛎糖胺聚糖 内皮细胞 过氧化氢 超氧化物歧化酶 oyster glycosaminoglycan endothelial cells hydrogen peroxide superoxide dismutase
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