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引用本文:王雪妹,王 晶,张全斌.褐藻多糖硫酸酯对脂多糖诱导大鼠肾小球系膜细胞NO产生量的影响[J].海洋科学,2014,38(10):1-5.
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褐藻多糖硫酸酯对脂多糖诱导大鼠肾小球系膜细胞NO产生量的影响
王雪妹1,2, 王 晶1, 张全斌1
1.中国科学院 海洋研究所 海洋生物技术工程研究发展中心;2.中国科学院大学
摘要:
慢性肾衰的进程中伴随着肾脏炎症的发生, 研究表明褐藻多糖硫酸酯具有抗炎作用, 且对于慢性肾衰的早期治疗具有一定的作用。本文通过脂多糖(lipopolysaccharide, LPS)诱导, 建立大鼠肾小球系膜细胞的炎症模型, 用来源于海带的高分子质量褐藻多糖硫酸酯F1 和低分子质量褐藻多糖硫酸酯F2对细胞进行处理, 24h后MTT法检测各组细胞活力, Griess法检测24h及48h后细胞培养液中NO的含量。结果表明, 各组间细胞活力无明显差异; 脂多糖可以诱导大鼠肾小球系膜细胞NO产量增加, F1和F2均可在一定程度上抑制脂多糖诱导的NO产量的增加, 从而减轻细胞炎症反应。剂量为25μg/mL的F1和F2处理细胞48h后, 与模型组相比, F1和F2组细胞培养液中NO含量分别下降22.52%和38.65%,低分子质量褐藻多糖硫酸酯抗炎效果明显高于高分子质量褐藻多糖硫酸酯。
关键词:  褐藻多糖硫酸酯  肾小球系膜细胞  脂多糖  一氧化氮  一氧化氮合酶
DOI:10.11759/hykx20131218002
分类号:
基金项目:国家自然科学基金项目(41376166); 江苏省科技支撑计划项目(BE2012687)
Effect of fucoidan on NO production induced by LPS in rat glomerular mesangial cells
Abstract:
The process of chronic renal failure is accompanied by renal inflammation. Fucoidan has anti-inflammatory activity, and therefore has potential effect for early treatment of chronic renal failure. In this paper, A inflammation model of rat glomerular mesangial cells was induced by lipopolysaccharide (LPS), then the cells were treated with high molecular fucoidan F1 and low molecular fucoidan F2 obtained from Laminaria japonica. After 24 h, the cell viability was detected by MTT method. After 24h and 48h, the content of NO in cell culture medium was detected by Griess method. The results show that, there was no difference in the cell viability among different groups. LPS could induce NO production by rat glomerular mesangial cells, and F1 and F2 could inhibit the NO production induced by LPS, thereby reducing the inflammatory response. The NO content in culture medium decreased 22.52% and 38.65%, respectively after treatment with 25 mg/L F1 and F2 for 48 h as compared with the control group. The anti-inflammatory effect of F2 is stronger than that of F1, suggesting the anti-inflammatory effect of low molecular fucoidan is higher than that of high molecular fucoidan.
Key words:  fucoidan  glomerular mesangial cells  Lipopolysaccharide  NO  NO synthase
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