[1]汤托,王胜男,蔡田雨,等.金盏花苷E通过ROS介导的JAK1-stat3信号途径抑制LPS诱发的炎症反应[J].南方医科大学学报,2019,(08):904.[doi:10.12122/j.issn.1673-4254.2019.08.05]
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金盏花苷E通过ROS介导的JAK1-stat3信号途径抑制LPS诱发的炎症反应()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2019年08期
页码:
904
栏目:
出版日期:
2019-08-31

文章信息/Info

Title:
Calenduloside E inhibits lipopolysaccharide- induced inflammatory response by inhibiting activation of ROS-mediated JAK1-stat3 signaling pathway in RAW264.7 cells
作者:
汤托王胜男蔡田雨程振宇齐世美戚之琳
关键词:
金盏花苷E脂多糖RAW264.7细胞炎症JAK1-stat3信号途径
Keywords:
calenduloside E lipopolysaccharide RAW264.7 cells inflammation JAK1-stat3 signaling pathway
DOI:
10.12122/j.issn.1673-4254.2019.08.05
摘要:
目的探讨金盏花苷E对脂多糖(LPS)诱导炎症反应的抑制作用及可能的分子机制。方法CCK-8实验检测不同浓度(0、 2、4、6、8、10、20、25、30 μg/mL)的金盏花苷E对RAW264.7 细胞活力的影响;不同浓度的金盏花苷E(0、6、8、10 μg/mL)预处理 RAW264.7细胞2 h,然后用LPS(100 ng/mL)刺激细胞特定的时间,ELISA检测炎症因子TNF-α、IL-1β释放;Western blotting检 测iNOS、COX-2的表达水平及JAK-stats、MAPKs及NF-кB信号途径的磷酸化;ROS检测试剂盒检测RAW264.7 细胞内ROS含 量;激光共聚焦实验检测转录因子stat3的核转位。结果CCK-8结果显示,金盏花苷E浓度在低于20 μg/mL时对RAW264.7细 胞无明显毒性作用;金盏花苷E浓度依赖性地下调LPS诱导的iNOS和COX-2的表达(P<0.01 vs LPS组);抑制LPS诱导的促炎 细胞因子TNF-α及IL-1β的释放,且1 0 μg/mL组抑制作用尤为显著(P<0.01 vs LPS组);抑制LPS诱导的JAK1-stat3信号途径激 活及stat3的核转位;降低LPS诱发的ROS产生(P<0.01 vs LPS组)。结论金盏花苷E通过抑制ROS介导的JAK1-stat3信号途 径,抑制LPS诱导的炎症反应。
Abstract:
Objective To investigate the effect of calenduloside E on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 cells and explore the underlying molecular mechanism. Methods CCK-8 assay was used to examine the effect of different concentrations of calenduloside E (0-30 μg/mL) on the viability of RAW264.7 cells. The release of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells in response to pretreatment with 6, 8, and 10 μg/mL calenduloside E for 2 h followed by stimulation with 100 ng/mL LPS was detected using enzyme-linked immunosorbent assay (ELISA). The expression levels of iNOS and COX-2 and the activation of JAK-stats, MAPKs and NF-кB signaling pathways in the treated cells were determined using Western blotting. A reactive oxygen species (ROS) detection kit was used to detect ROS production in the cells, and the nuclear translocation of the transcription factor stat3 was observed by laser confocal microscopy. Results Calenduloside E below 20 μg/mL did not significantly affect the viability of RAW264.7 cells. Calenduloside E dose-dependently decreased the expression levels of iNOS and COX-2 induced by LPS, inhibited LPS-induced release of TNF-α and IL-1β, and suppressed LPS-induced JAK1-stat3 signaling pathway activation and stat3 nuclear translocation. Calenduloside E also significantly reduced ROS production induced by LPS in RAW264.7 cells. Conclusion Calenduloside E inhibits LPS-induced inflammatory response by blocking ROS-mediated activation of JAK1-stat3 signaling pathway in RAW264.7 cells.

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更新日期/Last Update: 1900-01-01