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作 者:杨君[1] 沙前坤 李玉先[4] 陈瑾[5] 龙馨[1] 颜丽[1] 张华[1] YANG Jun;SHA Qian-kun;LI Yu-xian;CHEN Jin;LONG Xin;YAN Li;ZHANG Hua(Cervical Disease Treatment Center,Chongqing Health Center for Women and Children, Chongqing 400021, China;Dept of Pharmacy,Chongqing Yangdu Biology Institute, Chongqing 408000, China;Beibei Hospital of Chongqing Medical University, Chongqing 400700, China;Dept of Pharmacy,Chongqing Traditional Chinese Medicine Hospital, Chongqing 400011, China;Dept of Dermatology,the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China)
机构地区:[1]重庆市妇幼保健院宫颈疾病诊治中心,重庆400021 [2]重庆央都生物研究院药学部,重庆408000 [3]重庆医科大学北碚附属医院,重庆400700 [4]重庆市中医院药剂科,重庆400011 [5]重庆医科大学附属第一医院皮肤科,重庆400016
出 处:《中国药理学通报》2021年第12期1674-1679,共6页Chinese Pharmacological Bulletin
基 金:重庆市自然科学基金项目(No cstc2021jcyj-msxmX0718);国家自然科学基金资助项目(No 81372917);重庆市科技局与重庆市卫生健康委员会中医药课题(No 2020ZY023839)。
摘 要:目的探讨白藜芦醇苷(piceid,PD)通过MAPK和Nrf2/HO-1通路减轻脂多糖(lipopolysaccharides,LPS)引起的炎症反应的相关机制。方法采用MTT法测定PD在RAW264.7细胞中的细胞毒性,流式细胞术与蛋白印迹检测结果PD减少LPS引起的炎症反应与促炎细胞因子的表达,明显抑制p-JNK1/2、p-ERK1/2和p-p38MAPK的蛋白水平,明显抑制活性氧的生产和降低线粒体膜电位,提高细胞核中Nrf2蛋白水平,明显减弱LPS诱导的TLR4的表达。结论PD通过MAPK和Nrf2/HO-1通路对RAW264.7细胞表现出抗炎和抗氧化作用。Aim To investigate the mechanism of piceid reducing the inflammatory response caused by LPS through MAPK and Nrf2/HO-1 pathways.Methods MTT analysis was used to determine the cytotoxicity of piceid in RAW264.7 cells,flow cytometry and Western blot were used to detect the effect of piceid on inflammation,and flow and ELISA were applied to detect the effects of piceid on inflammatory factor levels.Western blot was used to detect the effect of piceid on MAPK and Nrf2/HO-1 pathways and Keap1-Nrf2 signaling pathways.Immunofluorescence and intracellular ROS kit were employed to assess the production of intracellular ROS,and immunofluorescence was used to evaluate its influence on mitochondrial membrane potential.Results Piceid reduced inflammatory reactions caused by LPS and the expression of pro-inflammatory cytokines,significantly inhibited the protein levels of p-JNK1/2,p-ERK1/2 and p-p38MAPK,markedly inhibited the production of reactive oxygen species and reduced the mitochondrial membrane potential,improved the Nrf2 protein level in the nucleus,and significantly weakened the expression of LPS-induced TLR4.Conclusions Piceid exhibits the anti-inflammatory and antioxidant effects on RAW264.7 cells through MAPK and Nrf2/HO-1 pathways.
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