脂氧素A4、保护素D1、ResolvinD1抑制多种激动剂引起的NFκB的活化

鲍华燕; 严君; 李珂; 刘鹏

doi:10.3969/j.issn.1006-0111.2012.03.008

留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

x 关闭永久关闭

应中央军委要求，2022年9月起，《药学实践杂志》将更名为《药学实践与服务》，双月刊，正文96页；2023年1月起，拟出版月刊，正文64页，数据库收录情况与原《药学实践杂志》相同。欢迎作者踊跃投稿！

脂氧素A4、保护素D1、ResolvinD1抑制多种激动剂引起的NFκB的活化

鲍华燕, 严君, 李珂, 刘鹏

文章导航 > 药学实践与服务 > 2012 > 30(3): 185-188

鲍华燕, 严君, 李珂, 刘鹏. 脂氧素A4、保护素D1、ResolvinD1抑制多种激动剂引起的NFκB的活化[J]. 药学实践与服务, 2012, 30(3): 185-188. doi: 10.3969/j.issn.1006-0111.2012.03.008

引用本文:

BAO Hua-yan, YAN Jun, LI Ke, LIU Peng. Stimulation of NFκB activity by the agonist inhibition from Lipoxin A4, Protectin D1 and Resolvin D1[J]. Journal of Pharmaceutical Practice and Service, 2012, 30(3): 185-188. doi: 10.3969/j.issn.1006-0111.2012.03.008

Citation:

BAO Hua-yan, YAN Jun, LI Ke, LIU Peng. Stimulation of NFκB activity by the agonist inhibition from Lipoxin A4, Protectin D1 and Resolvin D1[J]. Journal of Pharmaceutical Practice and Service, 2012, 30(3): 185-188. doi: 10.3969/j.issn.1006-0111.2012.03.008

脂氧素A4、保护素D1、ResolvinD1抑制多种激动剂引起的NFκB的活化

doi: 10.3969/j.issn.1006-0111.2012.03.008

中国医学科学院北京协和医学院药物研究所,北京 100050

基金项目: 国家自然科学基金重点项目(81030056);国家自然科学基金面上项目(30672468);中央级公益性科研院所基本科研业务费(2012CHX07).

Stimulation of NFκB activity by the agonist inhibition from Lipoxin A4, Protectin D1 and Resolvin D1

Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China

摘要: 目的探讨脂质小分子脂氧素A4 (LXA4)、保护素D1 (ProD1)、ResolvinD1 (RvD1) 对核因子κB (NFκB) 活性的影响及作用机制。方法稳定表达NFκB荧光素酶报告基因的中国仓鼠卵巢细胞分别由100 nmol/L LXA4、ProD1、RvD1预处理30 min后,细胞被激动剂LPS、HSP70、HMGB1或S100A4刺激。通过检测荧光素酶活性以评价脂质小分子对激动剂激活NFκB活性的作用。细胞培养上清中TNFα的含量由ELISA检测,胞核中NFκB的含量由Western
- 脂氧素A4 /
- 保护素D1 /
- resolvin /
- 核因子κB /
- 炎症
Abstract: Objective To examine effect of lipoxin A4 (LXA4), protectin D1 (ProD1) or resolvin D1 (RvD1) on the activity of NFκB and their action mechanism. Methods The CHO cells, stably expressing NFκB luciferase reporter gene, were treated with LPS, HSP70, HMGB1 or S100A4, in the presence or absence of 100 nmol/L of LXA4, ProD1 or RvD1 for 30 minutes. The activity of NFκB was detected with the luciferase assay. The content of tumor necrosis factor α (TNFα) in supernatant was measured by enzyme-1inked immunosorbent assay (ELISA) and the expression of NFκB in the nucleus was detected by immune blotting. Results The activity of NFκB and the level of TNFα in supernatant were significantly upregulated after treatment of the cells with LPS, HSP70, HMGB1 or S100A4, respectively. However, the NFκB activity and concentration of TNFα were lowered in the cells preincubated with LXA4, ProD1 or RvD1 as compared to the stimulated cells. Moreover, the lipids significantly decreased the content of NFκB in the nucleus. Conclusion LXA4, ProD1 or RvD1 could significantly inhibit the ligand-stimulated NFκB activity through interfering with NFκB translocation from cytoplast to nucleus. LXA4, ProD1 and RvD1 showed the potential in the development of new anti-inflammatory therapeutics, which was required further research.
- lipoxin /
- protectin /
- resolvin /
- NFκB /
- inflammation

[1]	Shames BD, Selzman CH, Meng XZ, et al. Genes don't count[J]. Arch Sung, 1998, 133(6):667.
[2]	Nemeth ZH, Hasko G, Vizi ES. Phrrolidine dithiocarbamate augments IL-10, inhibits TNF-alpha, MIP-1alpha, IL-12, and nitric oxide production and protects from the lethal effect of endotoxin[J]. Shock, 1998, 10(1):49.
[3]	Hamada N, Maeyama T, Kawaguchi T, et al.The role of high mobility group box l in pulmonary fibrosis[J].Am J Respir Cell Mol Biol,2008,39:440.
[4]	Vabulas RM,Ahmad NP,Ghose S,et al.HSP70 as endogenous stimulus of the Toll/interleukin-1 receptor signal pathway[J]. J Biol Chem, 2002, 277:15107.
[5]	Foell D,Frosch M,Sorg C,et al.Phagocyte-specific calcinm-binding S100 proteins as clinical laboratory markers of inflammation[J].Clin Chim Acta,2004,34:37.
[6]	Canny G, Levy O, Furuta GT, et al. Lipid mediator-induced expression of bactericidal/ permeability-increasing protein (BPI) in human mucosal epithelia［C］. Proc Natl Acad Sci USA, 2002, 99:3902.
[7]	Campbell EL, Louis NA, Tomassetti SE. et al. Resolvin E1 promotes mucosal surface clearance of neutrophils: a new paradigm for inflammatory resolution[J]. FASEB J, 2007, 21:3162.
[8]	Serhan, CN. A search for endogenous mechanisms of anti-inflammation uncovers novel chemical mediators: missing links to resolution[J]. Histochem Cell Biol, 2004, 122:305.
[9]	Bannenberg GL, Chiang N, Ariel A, et al. Molecular circuits of resolution: formation and actions of resolvins and protectins[J]. J Immunol, 2005, 174: 4345.
[10]	Serhan CN, Brain SD, Buckley CD, et al. Resolution of inflammation: state of the art, definitions and terms[J]. FASEB J, 2007,21:325.
[11]	Levy BD, Kohli P, Gotlinger K, et al. Protectin D1 is generated in asthma and dampens airway inflammation and hyperresponsiveness[J]. J Immunol, 2007, 178:496.
[12]	Duffield JS, Hong S, Vaidya VS, et al. Resolvin, series and protectin D1 mitigate acute kidney injury[J]. J Immunol, 2006, 177:5902.
[13]	Mitchell, S, Thomas G, Harvey K, et al. Lipoxins, aspirin-triggered epi-lipoxins, lipoxin stable analogues, and the resolution of inflammation: stimulation of macrophage phagocytosis of apoptotic neutrophils in vivo[J]. J Am Soc Nephrol, 2002, 13:2497.
[14]	Oeckinghaus A, Ghosh S. The NF-kappaB family of transcription factors and its regulation[J]. Cold Spring Harb Perspect Biol, 2009, 1(4):1.
[15]	Wang YP, Wu Y, Li LY,et al. Aspirin-triggered lipoxin A4 attenuates LPS induced pro-inflammatory responses by inhibiting activation of NFκB and MAPKs in BV-2 microglial cells[J]. J Neuroinflammation. 2011, 8: 95.
[16]	Serhan CN, Chiang N, Thomas E, et al. Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators[J]]. Nat Rev Immunol,2008,8(5):349.

[1]	杨嘉宁, 赵一颖, 肖伟. 七味脂肝方对非酒精性脂肪性肝炎动物模型的药效学评价 . 药学实践与服务, 2024, 42(9): 389-398. doi: 10.12206/j.issn.2097-2024.202404096
[2]	李想, 陆鸿远, 张明玉, 高欢, 姚东, 许子华. 米格列醇激活UCP1介导棕色脂肪对冷暴露小鼠损伤的研究 . 药学实践与服务, 2024, 42(): 1-6. doi: 10.12206/j.issn.2097-2024.202404005
[3]	刘汝雄, 杨万镇, 涂杰, 盛春泉. 铁死亡调控蛋白GPX4的小分子抑制剂研究进展 . 药学实践与服务, 2024, 42(9): 375-378. doi: 10.12206/j.issn.2097-2024.202312075
[4]	李丹, 戴贤春, 王芳珍, 陈奕含, 杨萍, 刘继勇. HPLC-MS/MS测定当归六黄汤中4种不同成分的含量 . 药学实践与服务, 2024, 42(6): 248-252, 266. doi: 10.12206/j.issn.2097-2024.202305007
[5]	毛智毅, 王筱燕, 陈晓颖, 汤逸斐. 度拉糖肽联合二甲双胍对肥胖型2型糖尿病患者机体代谢、体脂成分及血清脂肪因子的影响 . 药学实践与服务, 2024, 42(7): 305-309. doi: 10.12206/j.issn.2097-2024.202305032
[6]	岳春华, 贲永光, 王海桥. 基于NLRP1炎症小体探讨百合知母汤抗抑郁的作用机制 . 药学实践与服务, 2024, 42(8): 325-333. doi: 10.12206/j.issn.2097-2024.202401033
[7]	宋泽成, 陈林林, 鲁仁义, 刘梦肖, 王彦. 脓毒症治疗的研究进展 . 药学实践与服务, 2024, 42(11): 457-460, 502. doi: 10.12206/j.issn.2097-2024.202405059
[8]	张广雨, 杜晶, 刘梦珍, 朱丹妮, 闫慧, 刘冲. 新斯的明与山莨菪碱联合应用对肺型氧中毒的保护作用及其机制的研究 . 药学实践与服务, 2024, 42(10): 433-438, 444. doi: 10.12206/j.issn.2097-2024.202310049

点击查看大图

计量

文章访问数: 5397
HTML全文浏览量: 365
PDF下载量: 603
被引次数: 0

脂氧素A4、保护素D1、ResolvinD1抑制多种激动剂引起的NFκB的活化

doi: 10.3969/j.issn.1006-0111.2012.03.008

中国医学科学院北京协和医学院药物研究所,北京 100050

基金项目: 国家自然科学基金重点项目(81030056);国家自然科学基金面上项目(30672468);中央级公益性科研院所基本科研业务费(2012CHX07).

收稿日期: 2012-03-23
修回日期: 2012-05-07

关键词:

脂氧素A4 /

保护素D1 /

resolvin /

核因子κB /

炎症

摘要: 目的探讨脂质小分子脂氧素A4 (LXA4)、保护素D1 (ProD1)、ResolvinD1 (RvD1) 对核因子κB (NFκB) 活性的影响及作用机制。方法稳定表达NFκB荧光素酶报告基因的中国仓鼠卵巢细胞分别由100 nmol/L LXA4、ProD1、RvD1预处理30 min后,细胞被激动剂LPS、HSP70、HMGB1或S100A4刺激。通过检测荧光素酶活性以评价脂质小分子对激动剂激活NFκB活性的作用。细胞培养上清中TNFα的含量由ELISA检测,胞核中NFκB的含量由Western

English Abstract

Stimulation of NFκB activity by the agonist inhibition from Lipoxin A4, Protectin D1 and Resolvin D1

Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China

Received Date: 2012-03-23
Rev Recd Date: 2012-05-07

Keywords:

Abstract: Objective To examine effect of lipoxin A4 (LXA4), protectin D1 (ProD1) or resolvin D1 (RvD1) on the activity of NFκB and their action mechanism. Methods The CHO cells, stably expressing NFκB luciferase reporter gene, were treated with LPS, HSP70, HMGB1 or S100A4, in the presence or absence of 100 nmol/L of LXA4, ProD1 or RvD1 for 30 minutes. The activity of NFκB was detected with the luciferase assay. The content of tumor necrosis factor α (TNFα) in supernatant was measured by enzyme-1inked immunosorbent assay (ELISA) and the expression of NFκB in the nucleus was detected by immune blotting. Results The activity of NFκB and the level of TNFα in supernatant were significantly upregulated after treatment of the cells with LPS, HSP70, HMGB1 or S100A4, respectively. However, the NFκB activity and concentration of TNFα were lowered in the cells preincubated with LXA4, ProD1 or RvD1 as compared to the stimulated cells. Moreover, the lipids significantly decreased the content of NFκB in the nucleus. Conclusion LXA4, ProD1 or RvD1 could significantly inhibit the ligand-stimulated NFκB activity through interfering with NFκB translocation from cytoplast to nucleus. LXA4, ProD1 and RvD1 showed the potential in the development of new anti-inflammatory therapeutics, which was required further research.

引用本文: