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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 investigate the effects of curcumin on the inflammatory response of alveolar epithelial cells induced by lipopolysaccharide and the expression of single immunoglobulin (IL-1R) -related receptor protein. Methods: The type Ⅱ alveolar epithelial cells were cultured in vitro. The cell viability was measured after stimulation with lipopolysaccharide and curcumin. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL- 6) Level. After treated with 20μmol / L curcumin, 10μg / ml lipopolysaccharide (LPS) was added to stimulate the expression of nuclear protein and membrane protein, and to detect the expression of nuclear factor kappa B and mono-immunoglobulin interleukin-1. Results: Curcumin at 5 ~ 30μmol / L and lipopolysaccharide at 10μg / mL had no effect on cell viability (P> 0.05). Curcumin at 5 ~ 30μmol / L inhibited the production of TNF-α and IL-6 induced by LPS (P <0.05). The inhibitory effect of 20μmol / L and 30μmol / L curcumin was the most obvious, and there was no significant difference between the two groups (P> 0.05); 20μmol / L curcumin significantly reduced the intracellular nuclear phosphorylation The expression level of kappa B p65 (P <0.05) and the expression of monoimmunoglobulin interleukin-1receptor (IL-1R) -related protein (P <0.05) CONCLUSION: Curcumin can inhibit the release of inflammatory factors TNF-α and IL-6 and activation of NF-κB in rat type II alveolar epithelial cells induced by lipopolysaccharide, and up-regulate the expression of IL-1 IL-1R Related protein expression levels are one of the possible mechanisms.