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山东大学学报(医学版)

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葡萄籽原花青素对糖基化终产物损伤内皮细胞的保护作用

马丽,高海青,李保应,马亚兵   

  1. 山东大学齐鲁医院老年病科, 山东 济南 250012
  • 收稿日期:2006-11-17 修回日期:1900-01-01 出版日期:2007-06-24 发布日期:2007-06-24
  • 通讯作者: 高海青

Protective effects of grape seed proanthocyanidins on endothelial cells intervened by advanced glycosylation end products

MA Li, GAO Hai-qing, LI Bao-ying, MA Ya-bing   

  1. Department of Geriatrics, Qilu Hospital of Shandong University, Jinan 250012
  • Received:2006-11-17 Revised:1900-01-01 Online:2007-06-24 Published:2007-06-24
  • Contact: GAO Hai-qing

摘要: 目的:研究不同浓度葡萄籽原花青素(GSPC)对糖基化终产物(AGE)作用下人脐静脉内皮细胞的保护作用及其机制。 方法:体外培养人脐静脉内皮细胞(HUVEC),糖孵育法制备糖基化终产物修饰牛血清白蛋白(AGE-BSA)。实验分为6组,即空白对照组、实验对照组(BSA组)、损伤组(AGE组)、损伤加入GSPC低、中、高浓度组。将200mg/L AGE作用于不同浓度GSPC培养4h的内皮细胞,继续培养24?h,以细胞生存活力、血管性假血友病因子(vWF)、一氧化氮(NO)为检测指标。结果:200mg/L AGE抑制HUVEC生存活力,细胞增殖活力下降为正常组的90.53%,GSPC预孵育组细胞生存活力逐渐增加,分别为正常组的0.95、1.12、1.23倍;AGE组vWF生成量较正常对照组明显增加(P<0.01),NO含量较正常对照组明显降低(P<0.01)。GSPC预孵育组可显著降低增高的vWF水平,NO生成量显著高于AGE组(P<0.01), 100mg/L GSPC预处理组NO水平恢复至正常水平。结论:AGE会损伤内皮细胞,抑制内皮细胞的生存活力,减少NO的生成。GSPC可抑制AGE对内皮细胞的损伤作用,且可抑制AGE减少NO生成的作用,并呈浓度依赖性,提示GSPC保护内皮细胞免受AGE损伤的机制可能与增加内皮细胞NO生成量有关。

关键词: 一氧化氮, 葡萄籽原花青素 , 损伤, 高级, 内皮细胞, 糖基化终产物

Abstract: Objective:To investigate the protective effect of grape seed proanthocyanidins (GSPC) on human umbilical vein endothelial cells (HUVEC) injured by advanced glycosylation end products (AGE) and its possible mechanism. Methods: AGEmodified bovine serum albumin (AGEBSA) was prepared by incubating the BSA with a high concentration of glucose. The cultured HUVECs were divided into six groups: the control group,the BSA group, the AGE group, the low dose GSPC +AGE group, the middle dose GSPC+AGE group, and the high dose GSPC+AGE group. The cell proliferation of HUVEC, the Von Willebrand factor (vWF) and nitric oxide (NO) were determined. Results: After treatment with AGE, the proliferation of HUVEC was significantly reduced. The proliferation rate was 90.53% in the control group, while the proliferations of cells pretreated with GSPC of different concentrations were 0.95fold, 1.12fold, and 1.23fold that of the control group. The vWF level in AGEtreated HUVEC was higher than that of the control group (P<0.01). Preincubation with GSPC of different concentrations could decrease the vWF level increased by AGE in a dosedependent manner. The NO content in the AGEtreated group was significantly lower than that of the control group(P<0.01), while the AGEdecreased NO level was significantly increased in the GSPCpretreated groups. Conclusion: AGE can inhibit HUVEC proliferation, injure HUVEC and decreased the NO content. GSPC could protect HUVEC against damage induced by AGE and increase the NO level in the AGEexposed HUVEC. It is possible that the increased NO plays a key role in protecting the GSPC against damage induced by AGE.

Key words: Glycosylation end products, advanced, Endothelial cells, Injuries, Nitric oxide, Grape seed proanthocyanidin

中图分类号: 

  • R967
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