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机构地区:[1]第二军医大学海军临床医学院,北京市100048 [2]海军总医院呼吸科,北京市100048
出 处:《实用医学杂志》2017年第7期1070-1073,共4页The Journal of Practical Medicine
基 金:国家自然科学基金项目(编号:81300050);海军总医院创新培养基金项目(编号:CXPY201417)
摘 要:目的:探讨姜黄素对脂多糖诱导肺泡上皮细胞炎症反应及单免疫球蛋白白介素-1受体相关蛋白表达的影响。方法:体外培养大鼠Ⅱ型肺泡上皮细胞,用脂多糖及不同浓度姜黄素刺激后测定细胞活性;测定细胞上清中肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平。20μmol/L的姜黄素处理后加入10μg/m L的脂多糖刺激,提取细胞核蛋白及膜蛋白,检测核转录因子kappa B和单免疫球蛋白白介素-1相关蛋白的表达水平。结果:5~30μmol/L的姜黄素及10μg/m L脂多糖对细胞活性无影响(P>0.05);5~30μmol/L的姜黄素抑制脂多糖诱导的TNF-α和IL-6的产生(P<0.05),其中20μmol/L与30μmol/L姜黄素的抑制作用最为明显,且两组之间差异无统计学意义(P>0.05);20μmol/L的姜黄素显著降低细胞核内磷酸化核转录因子kappa B p65的表达水平(P<0.05),同时上调细胞内单免疫球蛋白白介素-1受体相关蛋白的表达(P<0.05)。结论:姜黄素可抑制脂多糖诱导的大鼠Ⅱ型肺泡上皮细胞炎性因子TNF-α和IL-6的释放以及核转录因子kappa B活化,上调负调控分子单免疫球蛋白白介素-1受体相关蛋白表达水平是可能的机制之一。Objective To explore the effect of eureumine on the inflammation and expression of single immunoglobin IL-1 receptor related protein in alveolar epithelial cells induced by lipopolysacharride (LPS). Methods The rat type Ⅱ alveolar epithelial cells were cultured in vitro, and cell activity was measured when stimulated with LPS and different doses of curcumin. The level of tumor necrosis factor-α (TNF-α) and interleukin- 6(IL-6) in supernatant was detected. Cells pretreated with curcumin (20 μmol/L), were stimulated with LPS (10μg/mL). The nuclear protein and membrane protein was extracted to detect the expression level of nuclear tran- scription factor kappa B (NF-KB) and single immunoglobin IL-1 receptor related protein (SIGIRR). Results The cells activities were not affected by eurcumin (5 -30μmol/L) and LPS (10 μg/mL) (P 〈 0.05 ). Curcumin (5 -30 μmol/L) significantly inhibited LPS-induced overpression of TNF-α and IL-6 (P 〈 0.05). In 20 μmol/L and 30 μmol/L pretreatment groups, the inhibition of curcumin was most obvious, and there were no significant differences between the two groups (P 〈 0.05 ). Curcumin (20 μmol/L) significantly inhibited the expression level of phosphorylation of NF-κB p65 in cell nucleus, while up-regulated the expression of SIGIRR (P 〈 0.05 ). Conclusion Curcumin inhibits the expression of inflammatory factor such as TNF-α and IL-6 as well as activation of NF-κB in alveolar epithelial cells induced by LPS. Up-regulating the expression level of negative regulatory molecules SIGIRR is one of the possible mechanism.
关 键 词:姜黄素 脂多糖 肺泡上皮细胞 炎症 单免疫球蛋白白介素-1相关蛋白
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