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

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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

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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: