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机构地区:[1]湖南中医药大学科技处,长沙410007 [2]中国中医科学院针灸研究所,北京100700 [3]湖南中医药大学第一附属医院检验科,长沙410007
出 处:《中华中医药杂志》2006年第12期730-733,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:湖南省教育厅科研基金重点资助项目(No.02A031)
摘 要:目的:探讨左归降糖灵改善葡萄糖、胰岛素和氧化型低密度脂蛋白联合诱导血管内皮细胞损伤的作用。方法:采用2型糖尿病血管并发症细胞研究模型,观察不同剂量左归降糖灵及达美康作用后细胞形态学、细胞生长活力及条件培养液中一氧化氮(NO)、内皮素1(ET-1)、组织型纤溶酶原激活物(tPA)、纤溶酶原激活物抑制物(PAI)含量的变化。结果:模型组细胞普遍回缩变圆,细胞内出现粗糙样颗粒变化,细胞活力明显下降(P<0.01),条件培养液中PAI和ET-1含量明显升高(P<0.01、0.05),NO含量明显降低(P<0.05),而tPA含量变化不明显(P>0.05);三个剂量的左归降糖灵组及达美康组均可不同程度改善细胞形态变化,提高细胞活力,降低PAI和ET含量,升高NO含量;除达美康组能提高tPA含量外,其余各组tPA变化不显著(P>0.05)。结论:左归降糖灵对葡萄糖、胰岛素和氧化型低密度脂蛋白联合诱导的血管内皮细胞形态学异常、细胞活力下降及调节血管舒缩和纤溶功能异常有显著的改善作用。Objective: To discuss the effects of Zuogui Jiangtangling extract on improving vascular endothelial cell damage induced by glucose, insulin and oxidized low-density lipoprotein Methods: Adopting the model of type 2 diabetic vascular complications cell research, the cell morphology, the cell growth vitality and the changes of NO, ET-1, tPA and PAI-1 in conditioned medium were observed after the actions of different dose of Zuogui Jiangtanging and diamicron. Results: In the model group, cells were general retraction and becoming rounded, rough particle-like changes appeared intra-cellular, the cell activity decreased significantly (P 〈0.01). The contents of ET-1 and PAl in conditioned medium were significantly increased (P 〈0.01, P 〈0.(15). NO were significantly lower (P 〈0.05), and tPA concentration did not change significantly (P〉0.05). Three doses of Zuogui Jiangtangling groups and the diamicron group may improve cell morphology changes, increase the cell activity, lower PAl and ET and increased NO in varying degrees. Except the high dose group of Zuogui Jiangtangling and the diamicron group can raise levds of tPA, tPA changes in the rest of the group was not significant (P 〉 0.05). Conclusion: Zuogui Jiangtangting has notahle improvement effects on morphology abnormity of vascular endothelial cell, decrease of the cell growth vitality, vasamotor regulation and fibronolysis abnormal induced by glucose, insulin and oxidized low-density lipoprotein.
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