论文部分内容阅读
目的 :观察雷公藤内酯醇对炎症因子刺激下人肾小管上皮细胞单核细胞趋化因子 (MCP 1)产生的影响。 方法 :以IFN γ(2 0 0 μg/L)及TNFα(2 0 μg/L)联合刺激人近端小管上皮细胞 ,细胞MCP 1蛋白含量以流式细胞仪检测 ,培养上清中MCP 1的分泌量以双抗体夹心ELISA法测定 ,细胞MCP 1mRNA含量采用半定量RT PCR法进行测定。 结果 :普通培养人近端肾小管上皮细胞及培养上清中有少量MCP 1分泌 ,IFN γ(2 0 0 μg/L)及TNFα(2 0μg/L)联合刺激 2 4h ,人近端小管上皮细胞合成MCP 1明显增加。雷公藤内酯醇可以抑制肾小管上皮细胞MCP 1分泌 ,并使细胞MCP 1mRNA含量明显降低 ,该抑制效应呈剂量依赖性。 结论 :雷公藤内酯醇可以抑制炎症刺激下人近端肾小管上皮细胞合成MCP 1,这可能是雷公藤内酯醇产生其疗效的机制之一。
Objective: To observe the effects of triptolide on the production of monocyte chemotactic factor (MCP 1) in human renal tubular epithelial cells stimulated by inflammatory cytokines. METHODS: Human proximal tubular epithelial cells were stimulated with IFNγ (200 μg / L) and TNFα (20 μg / L), and the MCP 1 protein level was detected by flow cytometry. The expression of MCP 1 The amount of secretion was measured by double antibody sandwich ELISA. The mRNA level of MCP 1 was determined by semi-quantitative RT-PCR. RESULTS: A small amount of MCP 1 secretion was induced in normal human proximal tubular epithelial cells and in culture supernatant. IFNγ (200 μg / L) and TNFα (20 μg / L) were stimulated for 24 hours. Human proximal tubular epithelial cells The cell synthesis of MCP 1 increased significantly. Triptolide inhibited MCP 1 secretion in renal tubular epithelial cells and significantly decreased MCP 1 mRNA expression in a dose-dependent manner. Conclusion: Triptolide can inhibit the synthesis of MCP 1 by human proximal tubular epithelial cells under inflammatory stimuli, which may be one of the mechanisms of triptolide production.