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作 者:张肇林[1] 梁艳红[1] 田铧[1] 肖琼 王世坤[1] 李鑫[1] 王雪颖[1] 田广平[1]
机构地区:[1]山东大学医学院解剖与组织胚胎学研究所,山东济南250012 [2]山东脐血库,山东济南250012
出 处:《中国现代普通外科进展》2010年第2期97-101,共5页Chinese Journal of Current Advances in General Surgery
基 金:山东省自然科学基金(ZR2009CZ014)
摘 要:目的:研究炎性因子TNF-α对大鼠骨髓间充质干细胞(MSCs)黏附分子表达及其干细胞特异性标志物的影响,探讨运用较少剂量的TNF-α诱导骨髓MSCs黏附分子的表达,促进其向肝缺血组织迁移。方法:用不同浓度的TNF-α刺激MSCs,检测其黏附分子的表达及干细胞标志物变化;取最佳浓度(10ng/mL)的TNF-α刺激MSCs,DiI标记后移植到肝脏缺血损伤的大鼠,检测大鼠肝功能,并取肝组织,荧光显微镜下计数组织中的MSCs。结果:1)MSCs受TNF-α刺激后,黏附分子VCAM-1表达升高,其表面干细胞标志物没有明显改变;2)10ng/mLTNF-α预刺激后,植到大鼠损伤肝组织内的MSCs数目明显多于对照组。结论:小浓度的TNF-α能够增强MSCs黏附分子VCAM-1的表达,且不影响大鼠骨髓MSCs干细胞的特性。大鼠体内实验证明TNF-α能促进MSCs的黏附,为治疗肝脏疾病提供理论基础。Objective: To study the influence of inflammatory cytokine TNF-α on the expression of adhesion molecules and specific markers of rat MSCs, and to study the optimal stimulation of MSCs with inflammatory factors in inducing adhesion molecule expression which promotes migration of MSCs to the ischemic area in liver. Methods: The MSCs stimulated with different concentration of TNF-α were detected for adhesion molecules and stem cells markers on cell surface with the method of flow-cytometry, MSCs which were stimulated with the optimal concentration of TNF-α and labeled with 1, 1-Dioctadecyl-3, 3, 3, 3-tetramethylindocarbocyanine Iodade(DiI)were delivered intravenously to the rats whose liver was injured by ischemia, the liver function of the experimented animals were tested, and liver samples in the ischemic area were obtained, the number of MSCs was counted under a fluorescent microscope. Results: Stimulated with TNF-α, MSC ex-pression of VCAM-1 increased, while that of stem cell markers did not change markedly. Exposed to lower concentration of TNF-α, the adhesion ability of MSCs obviously increased and more MSCs rested in the ischemic areas in the rat liver, compared to the control groups. Conclusions: TNF-α can increase the expression of VCAM-1 on rat MSCs while exert little effect on the stem cell character of MSCs. Suitable concentration of TNF-α can promote MSCs migration to the damaged tissue, which provides rationale for the treatment of liver disease.
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