文章摘要
孙 武,张欣欣,周文博,李 皓.蛇床子素抑制LPS诱导的肠上皮细胞株Caco2的炎症反应[J].南京医科大学学报,2017,(7):814~817
蛇床子素抑制LPS诱导的肠上皮细胞株Caco2的炎症反应
Osthole attenuates LPS-induced inflammatory response in Caco2 cells
投稿时间:2017-03-15  
DOI:10.7655/NYDXBNS20170706
中文关键词: 蛇床子素  脂多糖  炎症  MAPK  Caco2细胞
英文关键词: osthole  LPS  inflammation  MAPK  Caco2
基金项目:国家自然科学基金(81270944)
作者单位
孙 武 南京医科大学病理生理学系江苏 南京 211166 
张欣欣 南京医科大学病理生理学系江苏 南京 211166 
周文博 南京医科大学病理生理学系江苏 南京 211166 
李 皓 南京医科大学病理生理学系江苏 南京 211166 
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中文摘要:
      目的:探讨蛇床子素(osthole)对内毒素(lipopolysaccharide,LPS)诱导的肠上皮细胞Caco2中炎症因子表达的影响及机制。方法:培养Caco2细胞,用LPS诱导炎症反应。在LPS刺激前给予细胞不同浓度的蛇床子素处理,通过real-time PCR检测白介素(interleukin,IL)-1β、IL-6和肿瘤坏死因子(tumor necrosis factor,TNF)-α的表达情况。分别用PKA抑制剂H89和KT5720处理细胞,观察cAMP/PKA信号通路对蛇床子素效应的影响;用Western blot检测细胞中p38、Erk和JNK的磷酸化水平。结果:LPS刺激可以显著增加Caco2细胞中炎症因子IL-1β、IL-6和TNF-α的表达。蛇床子素预处理对LPS诱导的炎症反应有明显抑制作用,PKA抑制剂H89和KT5720不能逆转蛇床子素的抑制作用。LPS刺激后,Caco2细胞中p38、Erk和JNK的磷酸化水平明显增加,蛇床子素可部分抑制它们的磷酸化。结论:蛇床子素具有抑制肠上皮细胞株Caco2炎症反应的效应,该效应不依赖于cAMP/PKA,可能与抑制Erk、JNK和p38的磷酸化有关。
英文摘要:
      Objective:To investigate the effect of osthole on lipopolysaccharide (LPS)-induced inflammatory response in Caco2 cells and the underlying mechanism. Methods:Caco2 cells were treated with various concentrations of osthole prior to LPS treatment. The mRNA levels of interleukin (IL)-1β,IL-6 and TNF-α were detected by real-time PCR. Cells were treated with PKA inhibitors H89 or KT5720 prior to LPS at indicated doses to observe the effect of cAMP/PKA signaling pathway on osthole. The phosphorylations of p38,Erk and JNK were detected by Western blot. Results:The expressions of inflammatory factors IL-1β,IL-6 and TNF-α in Caco2 cells were significantly increased by LPS stimulation. Pretreatment of osthole significantly suppressed the up-regulation of inflammatory cytokines induced by LPS. PKA inhibitors failed to reverse the inhibitory effect of osthole. LPS induced significant phosphorylation of p38,Erk,and JNK in Caco2 cells,which were suppressed partly by osthole. Conclusion:Osthole attenuates LPS-induced nflammatory response in Caco2 cells. The inhibitory effect of osthole is independent on cAMP/PKA pathway. Osthole-induced reduction of phosphorylation of p38,Erk,and JNK may mediate its anti-inflammation action in Caco2 cells.
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