Li Xian-xia, Chen Shuang-xiu, Ye Qing-shan, Yu Li-ping, Cao Wei
Department of Pharmacy and Analysis, Yueyang Vocational and Technical College, Yueyang 414000, China.
Zhong Yao Cai. 2007 Sep;30(9):1109-13.
To explore the effect of extract of Ginkgo biloba (EGb) on vascular endothelial dysfunction induced by AGEs and to investigate the potential mechanisms.
Exogenous glycosylated bovine serum Albumin (AGEs-BSA) was prepared according to the methods of article. Vascular endothelial dysfunction was induced by tail vein injection of AGEs-BSA. The treatment group rats were given tail vein injections with AGEs-BSA followed by immediate intragastric of EGb (15,30 mg/kg/day, respectively) for 30 days. At the end of 30 days period, rats were anaesthetized with an intraperitoneal injection of sodium pentobarbital. Blood samples were collected from the carotid artery for biochemical assay of NO, MDA, SOD, DDAH, ADMA. The thoracic aorta was immediately isolated and cut into rings of 3 - 4 mm. Then ACh-induced EDR response and sodium SNP-induced endothelium-independent relaxation of aortic rings were examined.
Results from in vivo experiments showed that the injection of AGEs-BSA significantly inhibited ACh-induced EDR response, but had no effect on SNP-induced endothelial-independent relaxation. The injection of AGEs-BSA decreased concentration of serum NO, activity of serum SOD and elevated serum MDA and ADMA level. Egb markedly attenuated AGEs-BSA induced inhibition of EDR response, increase of serum MDA and ADMA level, reduction of both NO level and activity of serum SOD.
探讨银杏叶提取物（EGb）对晚期糖基化终末产物（AGEs）诱导的血管内皮功能障碍的影响，并研究其潜在机制。
按照文献方法制备外源性糖基化牛血清白蛋白（AGEs-BSA）。通过尾静脉注射AGEs-BSA诱导血管内皮功能障碍。治疗组大鼠尾静脉注射AGEs-BSA后，立即分别灌胃给予EGb（15、30mg/kg/天），持续30天。在30天结束时，腹腔注射戊巴比妥钠麻醉大鼠。从颈动脉采集血样，用于检测一氧化氮（NO）、丙二醛（MDA）、超氧化物歧化酶（SOD）、二甲基精氨酸二甲胺水解酶（DDAH）、不对称二甲基精氨酸（ADMA）的生化指标。立即分离胸主动脉并切成3-4mm的血管环。然后检测乙酰胆碱（ACh）诱导的内皮依赖性舒张反应（EDR）以及硝普钠（SNP）诱导的主动脉环内皮非依赖性舒张。
体内实验结果显示，注射AGEs-BSA显著抑制ACh诱导的EDR反应，但对SNP诱导的内皮非依赖性舒张无影响。注射AGEs-BSA降低了血清NO浓度、血清SOD活性，升高了血清MDA和ADMA水平。EGb明显减轻了AGEs-BSA诱导的EDR反应抑制、血清MDA和ADMA水平升高以及NO水平和血清SOD活性降低。
