木犀草素·4，4′ -联吡啶药物共晶对小鼠巨噬细胞RAW264.7的抗炎作用研究-中国药房

木犀草素·4，4′ -联吡啶药物共晶对小鼠巨噬细胞RAW264.7的抗炎作用研究

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篇名：	木犀草素·4，4′ -联吡啶药物共晶对小鼠巨噬细胞RAW264.7的抗炎作用研究
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摘要：	目的：研究木犀草素·4，4′ -联吡啶药物共晶的抗炎作用及机制。方法：以正常小鼠巨噬细胞RAW264.7为对照，以脂多糖（LPS）诱导的RAW264.7细胞为炎症模型，采用MTT法检测不同浓度（10、20、40、80 μmol/L）的木犀草素、4，4′ -联吡啶和木犀草素·4，4′ -联吡啶药物共晶作用细胞2 h后的细胞活性；荧光定量聚合酶链式反应法测定40 μmol/L浓度时细胞中诱导型一氧化氮合酶（iNOS）、环氧合酶2（COX-2）mRNA的表达，酶联免疫吸附法测定40 μmol/L浓度时细胞中肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）蛋白表达，Western blot法测定40 μmol/L浓度时细胞中核转录因子p65 （NF-κB p65）蛋白表达。结果：与正常细胞比较，LPS诱导后RAW264.7细胞活性明显降低（P＜0.01），iNOS和COX-2 mRNA表达水平及TNF-α、IL-6、NF-κB p65蛋白表达水平均明显升高（P＜0.01）。木犀草素和木犀草素·4，4′ -联吡啶药物共晶均能增强LPS诱导后RAW264.7细胞活性（P＜0.05或P＜0.01），且呈浓度依赖性；4，4′ -联吡啶对LPS诱导后RAW264.7细胞活性无明显影响；40 μmol/L浓度下，木犀草素和木犀草素· 4，4′ -联吡啶药物共晶可使LPS诱导后细胞中iNOS和COX-2 mRNA表达水平及TNF-α、IL-6、NF-κB p65蛋白表达水平明显降低（P＜0.05或P＜0.01），其中木犀草素·4，4′ -联吡啶药物共晶降低效果强于木犀草素（P＜0.05或P＜0.01）。结论：木犀草素·4，4′ -联吡啶药物共晶可能通过下调NF-κB信号来抑制炎症相关因子产生，其抗炎作用优于木犀草素。
ABSTRACT：	OBJECTIVE： To study anti-inflammatory effect and mechanism of the luteolin·4， 4′ -dipyridy co-crystal. METHODS： Using macrophage RAW264.7 of normal mice as control， the inflammation model was established with lipopolysaccharide （LPS）-induced RAW264.7 cells. MTT assay was used to detect cells activity 2 h after treatment of different concentrations of luteolin （10， 20， 40， 80 μmol/L）， 4， 4′ -dipyridy （10， 20， 40， 80 μmol/L） and luteolin·4， 4′ -dipyridy co-crystal （10， 20， 40， 80 μmol/L）. The mRNA expression of iNOS and COX-2 in RAW264.7 cells at 40 μmol/L were determined by qRT-PCR. The protein expression of TNF-α and IL-6 in RAW264.7 cells at 40 μmol/L were determined by ELISA. The protein expression of NF-κB p65 in RAW264.7 cells at 40 μmol/L were determined by Western bolt. RESULTS： Compared with normal cells， the activity of RAW264.7 cells was decreased significantly after induced by LPS （P＜0.01）； mRNA expression of iNOS and COX-2， protein expression of TNF-α， IL-6 and NF-κB p65 were increased significantly （P＜0.01）. Both luteolin and luteolin· 4， 4′ -dipyridy co-crystal could enhance the activity of RAW264.7 cells after induced by LPS （P＜0.05 or P＜0.01） in concentration-dependent manner. 4， 4′ -dipyridy had no significant effect on the activity of RAW264.7 cells after induced by LPS. After luteolin and luteolin·4， 4′ -dipyridy co-crystal at 40 μmol/L， mRNA expression of iNOS and COX-2， protein expression of TNF-α， IL-6 and NF-κB p65 in RAW264.7 cells after induced by LPS were decreased significantly （P＜0.05 or P＜0.01）； the luteolin·4， 4′ -dipyridy co-crystal was better than luteolin （P＜0.05 or P＜0.01）. CONCLUSIONS： The luteolin·4， 4′ -dipyridy co-crystal can inhibit the generation of inflammatory factors by down-regulating NF-κB signal， and its anti-i nflammatory effect is better than luteolin.
期刊：	2018年第29卷第5期
作者：	刘立新，邹冬玉，张羽男，张强，张楠楠
AUTHORS：	LIU Lixin，ZOU Dongyu，ZHANG Yunan，ZHANG Qiang，ZHANG Nannan
关键字：	木犀草素；4，4′ -联吡啶；药物共晶；小鼠巨噬细胞RAW264.7；抗炎作用
KEYWORDS：	Luteolin； 4， 4′ -dipyridy； Pharmaceutical co-crystal； Mice macrophage RAW264.7； Anti-inflammatory effect
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