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ZD制剂对RAW264.7细胞分泌TNF-α水平及TNF-α诱导L929细胞死亡的影响
引用本文:蒋瑞东,高鑫,李云章.ZD制剂对RAW264.7细胞分泌TNF-α水平及TNF-α诱导L929细胞死亡的影响[J].畜牧与饲料科学,2018,39(5):7-7.
作者姓名:蒋瑞东  高鑫  李云章
作者单位:内蒙古农业大学兽医学院,内蒙古呼和浩特010018
基金项目:国家自然科学基金项目(31360629).
摘    要:目的]研究ZD制剂对炎症模型细胞中TNF-α含量及对TNF-α诱导小鼠成纤维细胞L929死亡的影响。方法]通过脂多糖(LPS)刺激小鼠腹腔巨噬细胞RAW264.7细胞系来构建炎症细胞模型,使用5种不同浓度(100、10、1、0.1、0.01μg/m L)的ZD制剂进行试验,并用ELISA法检测ZD制剂干预前后细胞上清液中TNF-α浓度。通过TNF-α刺激小鼠成纤维细胞L929细胞系来构建细胞毒性模型,采用MTT法检测ZD制剂干预前后L929细胞活力。结果]ZD制剂浓度为100、10、1、0.1μg/m L时,TNF-α浓度与LPS模型组相比,差异极显著(P〈0.01);ZD制剂浓度为0.01μg/m L时,TNF-α浓度与LPS模型组相比,差异显著(P〈0.05)。经100、10μg/m L ZD制剂干预后的小鼠成纤维细胞L929细胞活力与TNF-α组相比显著提高。结论]ZD制剂可以通过降低TNF-α的分泌量和降低TNF-α的生物学活性来达到抗炎的目的。


Effects of ZD Preparation on Secretion of TNF-α by RAW264.7 Cells and TNF-αInduced L929 Cells Death
Abstract:Objective]To study the effects of ZD preparation on the concentration of TNF-α in a cellular model of inflammation and the death of mouse fibroblast L929 cells induced by TNF-α. Methods] The mouse peritoneal macrophage RAW264.7 cell line was stimulated by lipopolysaccharide(LPS) to establish a cellular model of inflammation, and five different concentrations of ZD preparation(100, 10, 1, 0.1, 0.01 μg/m L) were included in this study. ELISA method was used to detect the TNF-αconcentration in the cell supernatant before and after ZD preparation intervention. The cytotoxic model was established with mouse fibroblast L929 cell line by stimulation of TNF-α, and the activity of L929 cells was determined by MTT method before and after the intervention of ZD preparation. Results] The 100, 10, 1 and 0.1 μg/m L of ZD preparation groups had extremely significant difference in TNF-α concentration compared to the LPS model group(P〈0.01), and the 0.01 μg/m L of ZD preparation group showed significant difference in TNF-α concentration compared to the LPS model group(P〈0.05). In addition, the activity of mouse fibroblast L929 cells were significantly elevated after the intervention of 100 and 10 μg/m L of ZD preparation compared to the TNF-α group. Conclusion] ZD preparation exerts the anti-inflammatory effects via reducing the secretion of TNF-α and inhibiting the biological activity of TNF-α.
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