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作 者:游洋[1,2] 段岩[2] 张效林[2] 康建[2] 闫承慧[2] 张秀莉[3] 丰加涛[3] 韩雅玲[2]
机构地区:[1]辽宁中医药大学附属医院,辽宁省沈阳市110032 [2]沈阳军区总院心研所,辽宁省沈阳市110840 [3]中国科学院大连化学物理研究所,辽宁省大连市116023
出 处:《中国动脉硬化杂志》2011年第3期187-191,共5页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金项目(30770793;30971218;81070097);辽宁省自然基金项目(20092088)资助
摘 要:目的探讨黄芪水提取物对肿瘤坏死因子α(TNF-α)诱导的小鼠动脉内皮细胞VCAM-1表达的影响及机制。方法建立体外THP-1细胞与小鼠动脉内皮细胞黏附实验体系,在施加TNF-α刺激之前,采用不同浓度黄芪水提取物及不同预先黄芪水提取物孵育时间进行分组干预,并检测THP-1细胞对小鼠动脉内皮细胞的黏附率;ELISA检测细胞培养上清液中VCAM-1表达的变化。Western blot检测VCAM-1表达的变化及核转录因子NF-κB p65蛋白的核转运。结果 TNF-α刺激下,小鼠动脉内皮细胞VCAM-1和NF-κB的表达水平显著升高,而经黄芪水提取物预处理后,可具有抑制TNF-α诱导的VCAM-1表达及NF-κB p65蛋白核转移的作用,并表现一定剂量依赖性及时间依赖性,其中120 mg/L的黄芪水提取物预孵4~8 h可明显减少单核细胞对内皮细胞的黏附率,VCAM-1表达明显下调(P<0.05),NF-κB表达明显降低(P<0.05)。结论黄芪水提取物可拮抗TNF-α诱发的内皮细胞VCAM-1的表达,降低单核细胞的黏附能力,从而减轻血管内皮细胞损伤,其机制可能通过抑制转录因子NF-κB的活化有关。Aim To investigate the protective effect of Astragali radix extract on vascular cell adhesion molecule-1 expression of mice vascular endothelial cell against tumor necrosis factor-α(TNF-α). Methods Adhesion model was established by THP-1 cells and mice endothelial cell in vitro.The cells were pretreated by different dose and different time of Astragali radix extract before induced by TNF-α,and the adhesion rate were detected.The levels of vascular endothelial cell adhesion molecule VCAM-1 in the cell culture were determined with ELISA.The expression of VCAM-1 and NF-κB subunit(p65) were evaluated by Western blot. Results The expression of VCAM-1 and NF-κB was increased obviously after induced by TNF-α;While the expression of VCAM-1 and the effect of NF-κB p65 protein nuclear translocation induced by TNF-α were inhibited after pretreatment of Astragali radix extract in a dose-and time-dependent manner.The reduction of adhension of monocytes to endothelial cells,the down-regulation of the expression of VCAM-1 and reduc-tion of the expression of NF-κB were apparent(P0.05) at the concentration of 120 mg/L preincubated 4~8 h. Conclusion Astragali radix extract can inhibit the TNF-α-induced expression of VCAM-1 and reduce the adhension of monocytes,by which the damage to vascular endothelial cells was relieved.The mechanism may be related to the role of inhibiting the activation of NF-κB.
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