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冬凌草甲素增强巨噬细胞对凋亡的U937细胞的吞噬作用

Oridonin enhances phagocytosis of apoptotic U937 cells by macrophage-like cells

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【作者】 刘艳秋游松张春玲田代真一小野寺敏池岛乔

【Author】 LIU Yan-qiu~ 1,2 , YOU Song~2, ZHANG Chun-ling~1, TASHIRO Shin-ichi~3, ONODERA Satoshi~3, IKEJIMA Takashi~1 (~1China-Japan Research Institute of Medical and Pharmaceutical Sciences,~2Laboratory of Natural Product Biotechnology, Shenyang Pharmaceutical University, Shenyang 110016, China;~3Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan)

【机构】 沈阳药科大学中日医药研究所沈阳药科大学天然产物生物技术实验室昭和药科大学病态科学教研室沈阳药科大学中日医药研究所 沈阳药科大学天然产物生物技术实验室辽宁沈阳110016东京194-8543日本国

【摘要】 目的:研究具有诱导肿瘤细胞凋亡活性的冬凌草甲素,促进巨噬细胞对因凋亡的肿瘤细胞的吞噬作用。方法:DNA凝胶电泳检测UV照射(2·4J/cm2,4min)的人组织淋巴瘤U937细胞凋亡;Giemsa染色,Hoechst33258染色,镜下检测计数吞噬作用。结果:UV照射(2·4J/cm2,4min)诱导U937细胞发生凋亡,琼脂糖凝胶电泳可见凋亡典型的DNA梯带。2·7μmol·L-1的冬凌草甲素具有增强U937分化的巨噬细胞对UV照射诱导凋亡的U937细胞的吞噬作用,并呈时间剂量依赖性,但对非特异性荧光颗粒的吞噬效果较弱。加入抗TNFα和抗IL-1β的抗体,培养12h,吞噬增强作用明显受抑制。冬凌草甲素在人外周血来源的巨噬细胞吞噬凋亡的U937细胞过程中同样发挥增强吞噬的效果。结论:冬凌草甲素可特异地增强巨噬细胞对凋亡的U937细胞的吞噬作用,其吞噬机制是通过诱导巨噬细胞TNFα和IL-1β的释放。

【Abstract】 AIM: To study the effect of oridonin on the phagocytosis of apoptotic U937 cells by macrophage-like cells. METHODS: DNA agarose gel electrophoresis, Giemsa staining, Hoechst 33258 staining and photomicroscopical observation were used. RESULTS: UV irradiation (2.4 J/cm~2, 4 min) induced U937 cell apoptosis. Marked DNA fragmentation in agarose gel electrophoresis was observed. Oridonin augmented phagocytosis of apoptotic U937 cells by U937 cell-derived macrophages in a time- and dose-dependent manner. However, less effect on synthetic fluoresbrite micropheres was observed. The oridonin-augmented phagocytosis was attenuated by anti-human TNFα or anti-human IL-1β antiserum. In addition, the similar effect of phagocytosis was observed in oridonin-treated human monocyte-derived macrophages at 4 day maturation. CONCLUSION: Oridonin enhances phagocytosis of apoptotic U937 cells by macrophage-like cells. The releases of TNFα and IL-1β are involved in this mechanism.

  • 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,2006年02期
  • 【分类号】R285.5
  • 【被引频次】13
  • 【下载频次】309
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