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作 者:孔田玉[1] 张振辉[1] 胡欢[1] 辜洪娇 熊旭明[1]
机构地区:[1]广州医科大学附属第二医院重症医学科,广东广州510260
出 处:《中国急救医学》2016年第4期362-366,共5页Chinese Journal of Critical Care Medicine
基 金:广东省科技厅项目(20128031800233)
摘 要:目的探讨高良姜素对脂多糖(LPS)诱导人急性单核细胞白血病细胞株THP-1细胞炎症的保护作用及其可能的机制。方法MTS法检测细胞活性;酶联免疫吸附(ELISA)法检测TNF-α、MCP-1、IL-1β、IL-6的分泌;免疫印迹(Western blot)法检测NF—κB以及MAPK通路相关蛋白的变化。结果高良姜素在0~20μmol/L范围内对细胞活力无明显影响。LPS的用药浓度为500ng/mL;与LPS模型组相比,高良姜素2.5~20μmol/L能有效抑制炎症因子TNF-α、MCP-1、IL-1β、IL-6的释放(P〈0.05);高良姜素20μmol/L能抑制NF—κB通路IKBα的磷酸化,从而减少核转录因子(NF)-κB的核转位,但对MAPK通路无影响。结论高良姜素对LPS刺激的THP-1细胞炎症具有一定的保护作用,其保护机制可能与其调控NF—κB通路,抑制IKBa的磷酸化,减少NF-κB的核转录,进而抑制TNF-α、MCP-1、IL-1β、IL-6的表达有关。Objective To observe the protective effect of galangin on the inflammation of human monocytic THP- 1 cells induced by lipopolysaccharide (LPS) and to explore it's underlying mechanisms. Methods Cell viability was detected by MTS method; ELISA was used to detect the expression of tumor necrosis factor- α (TNF-α), monocyte chemotactic protein 1 (MCP- 1 ), interleukin 1β (IL- 1β ) and interleukin 6 (IL-6). The changes in protein levels of NF-κB and MAPK signal pathway were detected by Western blot. Results Galangin within 0-20 μmol/L had no effect on cell viability. Concentration of LPS was 500 ng/mL. Compared with the LPS model group, 2.5-20 μmol/L of galangin could inhibit the release of TNF-α, MCP-1, 1L-1β, IL-6 (P 〈 0.05). 20 μmol/L of Galangin could inhibit the phosphorylation of IκBα, reduce the occurrence of NF-κB nuclear translocation. However, the protein levels of MAPK signal pathway were unaltered by galangin. Conclusion Galmagin has protective effects on THP-1 cells stimulated by LPS. The mechanism of galangin may be related to regulating the NF-κB signal pathway, inhibiting the phosphorylation of IκBα, reducing the occurrence of NF-κB nuclear translocation, thereby inhibiting the release ofTNF-α, MCP-1, IL-1β and IL-6.
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