摘要
目的:探讨树突状细胞(DC)在中药方剂通心络(TXL)对血管紧张素Ⅱ(Ang Ⅱ)引起的小鼠内皮细胞损伤过程中的作用. 方法:C57BL/6小鼠随机分为假手术组(Sham组),血管紧张素Ⅱ组(Ang Ⅱ组),通心络保护组(Ang Ⅱ+TXL组).扫描电镜观察胸主动脉内皮的损伤状况;流式细胞术检测外周血液中单个核细胞CD11c的表达及胫、腓骨骨髓中树突状细胞的前体细胞标志ER-MP58的表达.免疫组织化学法检测胸主动脉壁、心肌间质、肾皮质中S100的表达.结果:电镜显示Ang Ⅱ+TXL组血管壁上内皮细胞的损伤明显较Ang Ⅱ组减轻,骨髓中ER-MP58及血液中CD11c表达水平明显降低,胸主动脉壁、心肌间质、肾皮质中S100阳性细胞数减少.结论:通心络可通过抑制骨髓中DCs前体细胞的数量,减少DCs在组织、血液中的水平,对血管紧张素Ⅱ导致的小鼠血管内皮损伤发挥保护作用.
Objective: To evaluate the protective effect of tongxinluo (TXL) on vascular endothelium injured by angiotensin Ⅱ in mice and the changes of the dendritic cells (DC). Methods: C57BL/6 mice were randomly divided into three groups: a sham group, AngiotensinⅡ treated group (Ang Ⅱ group), Ang Ⅱ treated and Tongxinluo pretreated group (Ang Ⅱ+ TXL group, TXL pretreated 3 days in advance). Angiotensin Ⅱ osmotic pump at a dose of 200 ng ·min^-1 · kg-1 were em- bedded in the mice back in the Ang Ⅱ group and the Ang Ⅱ +TXL group, whereas physiological saline osmotic pump in the sham group. Tongxinluo (0. 8 g · kg^- 1 · d ^-1 ) treated group was given by gastric tube every day. All animals were sacrificed at the 14th day. The morphology of endothelial cell in the thoracic aorta was observed under a scanning electron microscope. ER-MP58 from bone marrow and CD11c from plasma were analyzed via flow cytometry. S100 expressions in the aorta, car- diac muscle and kidney were measured by immunohistochemistry. Results: ER-MP58, CD11c and S100 were significantly highly expressed in the Ang Ⅱ group, which could be significantly attenuated by TXL. Conclusion: TXL could protect the endothelium against the injury from angiotensin Ⅱ by inhibiting the numbers of DC precursor (ER-MP58) in bone marrow and mature DCs in the blood (CDllc) and in the vascular wall (S100).
出处
《解剖学杂志》
CAS
CSCD
北大核心
2010年第4期428-431,共4页
Chinese Journal of Anatomy
基金
国家重点基础研究发展计划(2005CB523302)