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作 者:詹杰[1,2] 刘永林[2] 柳承希[1] 魏树和[3] 张静生[1]
机构地区:[1]辽宁中医药大学,辽宁沈阳110032 [2]辽宁省基础医学研究所,辽宁沈阳110101 [3]中国科学院沈阳应用生态研究所,辽宁沈阳110016
出 处:《辽宁中医杂志》2011年第7期1457-1459,共3页Liaoning Journal of Traditional Chinese Medicine
基 金:辽宁省科技厅课题(2004226010-520040278);国家自然科学基金面上项目(31070455;40971184)资助
摘 要:目的:对比观察冠心康和锌对镉染毒人脐静脉内皮细胞NO水平和细胞增殖率的变化,分析其抗镉染毒致动脉粥样硬化的可能途径。方法:人脐静脉内皮细胞体外培养,随机分为空白组、模型组、补锌组,及冠心康低、中、高剂量组,分别以空白血清、CdCl2血清、CdCl2及硫酸锌血清和CdCl2及冠心康血清培养24h、48h、72h,收集培养液,硝酸还原酶法测定NO浓度,MTT法检测细胞增值率;结果:1μM、5μM、10μM、30μM和60μM各组镉染毒HUVECS细胞NO水平明显下降(P<0.01),60μΜ镉染毒浓度可致HUVECs细胞增殖率(PR)显著降低(P<0.01);而与模型组相比,冠心康组、补锌组的NO含量和PR均有明显恢复(P<0.01)。结论:①冠心康可明显提高镉染毒HUVECs的NO和PR,从而减少血管内皮损伤,发挥抗动脉粥样硬化作用;②气虚痰瘀可能是镉染毒诱发动脉硬化的主要病机。Objective:To observe the protective effect of Guanxinkang Powder(GXK) on nitric oxide(NO) generation of cadmium(Cd) exposed human umbilical vein endothelial cells(HUVECs),and study its possible anti-atherosclerotic mechanism.Methods:The HUVECs were divided into 6 groups:normal control group,model group,zinc group and 0.8g/mL,1.6g/mL,3.2g/mL GXK groups.Except the control group,the injured cell models of HUVECs of each group were established by exposure with 1μM,5μM,10μM,30μM,60μM Cd.Simultaneously cultured with normal,zinc,or 0.8g/mL,1.6g/mL,3.2g/mL GXK serum of rat.Cells in each group were treated for 24,48 and 72 hours of feeding,respectively,NO concentration of culture serum and the vascular epithelial cell proliferation rate(PR) were measured.Results:Compared with the control group,the HUVECs of model group with 1μM,5μM,10μM,30μM,60μM Cd exposed serum culturing showed lower NO concentration and decreased PR of the endothelial cell(P0.01).In contrast,Compared with the model group,zinc group and 0.8g/mL,1.6g/mL,3.2g/mL GXK groups were higher PR with recovery of the NO level(P0.01).Conclusion:NO deficiency and PR decrease are involved in HUVECs impairment induced Cd,and GXK powder can effectively prevent atherosclerosis by restoring NO concentration and increasing the vascular epithelial cell PR.
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