云南中医学院学报
雲南中醫學院學報
운남중의학원학보
JOURNAL OF YUNNAN COLLEGE OF TRADITIONAL CHINESE MEDICINE
2013年
6期
22-25
,共4页
姜黄素%TLR4 mRNA%肿瘤坏死因子%脂多糖
薑黃素%TLR4 mRNA%腫瘤壞死因子%脂多糖
강황소%TLR4 mRNA%종류배사인자%지다당
Curcumin%TLR4 mRNA%TNF-a%LPS
目的:研究姜黄素对原代培养的肺巨噬细胞表达TLR4mRNA及分泌TNF-a、IL-6和IL-8的影响。方法用脂多糖(LPS)建立体外肺巨噬细胞体外炎症损伤模型,用ELISA观察肺巨噬细胞分泌TNF-a、IL-6和IL-8和用RT-PCR、western blot观察肺巨噬细胞TLR4的表达。结果 LPS明显诱导肺巨噬细胞分泌TNF-a、IL-6和IL-8增加及TLR4的增量表达(P<0.01),姜黄素可抑制这种作用(P<0.05),且与姜黄素药物浓度有关(P>0.05)。结论姜黄素对肺巨噬细胞的抗炎机制可能是通过抑制TLR4的表达,通过脂多糖-TLR4信号传导通路,从而减少炎性细胞因子的释放;姜黄素有可能作为一种有研究潜力的抗感染治疗的中药。
目的:研究薑黃素對原代培養的肺巨噬細胞錶達TLR4mRNA及分泌TNF-a、IL-6和IL-8的影響。方法用脂多糖(LPS)建立體外肺巨噬細胞體外炎癥損傷模型,用ELISA觀察肺巨噬細胞分泌TNF-a、IL-6和IL-8和用RT-PCR、western blot觀察肺巨噬細胞TLR4的錶達。結果 LPS明顯誘導肺巨噬細胞分泌TNF-a、IL-6和IL-8增加及TLR4的增量錶達(P<0.01),薑黃素可抑製這種作用(P<0.05),且與薑黃素藥物濃度有關(P>0.05)。結論薑黃素對肺巨噬細胞的抗炎機製可能是通過抑製TLR4的錶達,通過脂多糖-TLR4信號傳導通路,從而減少炎性細胞因子的釋放;薑黃素有可能作為一種有研究潛力的抗感染治療的中藥。
목적:연구강황소대원대배양적폐거서세포표체TLR4mRNA급분비TNF-a、IL-6화IL-8적영향。방법용지다당(LPS)건입체외폐거서세포체외염증손상모형,용ELISA관찰폐거서세포분비TNF-a、IL-6화IL-8화용RT-PCR、western blot관찰폐거서세포TLR4적표체。결과 LPS명현유도폐거서세포분비TNF-a、IL-6화IL-8증가급TLR4적증량표체(P<0.01),강황소가억제저충작용(P<0.05),차여강황소약물농도유관(P>0.05)。결론강황소대폐거서세포적항염궤제가능시통과억제TLR4적표체,통과지다당-TLR4신호전도통로,종이감소염성세포인자적석방;강황소유가능작위일충유연구잠력적항감염치료적중약。
Objective To study the influence of Curcumin on the expressions of TLR4 and TNF-a、IL-6 、IL-8 release in pulmonary macrophage. Methods The experiments were performed in culture of LPS induced pulmonary macrophage in vitro,the TNF-a、IL-6 、IL-8 release was detected with ELISA and the expressions of TLR4 was detected with RT-PCR and western blot. Results Pulmonary macrophage was stimulated with LPS and the expressions of TLR4 and TNF-a 、IL-6、IL-8 release was increased (P<0.01),but it was inhibited by Curcumin (P<0.05),and dose dependence (P<0.05). Conclusion The mechanism of Curcumin’s antiinflammatory may be reduce cytokine release,by inhibits expressions of TLR4 and via Cross talk toll-like receptor-4 signaling;Curcumin may be used as a kind of anti-infective drug.