脱水淫羊藿素对腹膜炎小鼠的保护作用  被引量:2

Protective effect of anhydroicaritin against peritonitis in mice

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作  者:赖新强[1] 黄秀艳[2] 曾耀英[2] 

机构地区:[1]暨南大学分析测试中心,广东广州510632 [2]暨南大学组织移植与免疫中心

出  处:《细胞与分子免疫学杂志》2013年第10期1036-1039,共4页Chinese Journal of Cellular and Molecular Immunology

基  金:国家自然科学基金(31200667)

摘  要:目的研究脱水淫羊藿素(AHI)对酵母多糖诱导的小鼠腹膜炎的影响。方法采用酵母多糖诱导腹膜炎模型,观察各组小鼠的生存情况,收集腹腔液,分别进行白细胞计数,Griess试剂联合酶标仪检测一氧化氮(NO)、流式细胞术检测小鼠腹腔渗出液中IL-6、IL-10、TNF-α、单核细胞趋化蛋白1(MCP-1)的水平;采用Fluo4-AM标记,激光扫描共聚焦显微镜实时检测AHI对骨髓巨噬细胞钙离子内流的影响;Western blot法检测AHI对一氧化氮合酶(iNOS)的影响。结果 4 mg/kg体质量的AHI能提高腹膜炎小鼠的存活,减少腹腔白细胞的数量,降低NO、IL-10、TNF-α、MCP-1、IL-6的分泌;5μmol/L的AHI能抑制小鼠巨噬细胞的钙内流和iNOS的表达。结论 AHI对酵母多糖诱导的腹膜炎小鼠具有保护作用,可能与抑制巨噬细胞的钙离子内流、iNOS表达有关。Objective To investigate the effect of anhydroicaritin (AHI) against zymosan-induced peritonitis in mice. Methods Peritonitis was induced in mice by intraperitoneal injection of zymosan. All mice were monitored for systemic toxicity and mortality for 13 d after zymosan or saline administration. In another set of experiments, the peritoneal exudates were collected. The leukocyte numbers and the production of inflammatory cytokines (IL-6, IL-10, TNF-α, MCP-1) were determined by flow cytometry. The release of nitric oxide (NO) was measured by a Griess reagent system. The Ca2+ influx in bone marrow-derived macrophages was recorded by laser scanning confocal microscopy with Fluo4-AM loading. The expression of iNOS was determined by Western blotting. Results AHI (4 mg/kg) prolonged survival of peritonitis mice, inhibited massive leukocyte transmigration into the peritoneal cavity, and decreased the overproduction of NO, IL-10, TNF-α, MCP-1 and IL-6. In LPS-stimulated mouse macrophages, AHI (5 μmol/L) pretreatment significantly inhibited the elevation of intracellular Ca2+, and markedly decreased iNOS protein expression. Conclusion AHI possesses significant protective effects on the zymosan-induced peritonitis mice, which might be associated with the regulation of Ca2. influx in macrophages and iNOS expression.

关 键 词:脱水淫羊藿素 腹膜炎 酵母多糖 巨噬细胞 

分 类 号:R392.12[医药卫生—免疫学] R572.2[医药卫生—基础医学]

 

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