Anti-inflammatory function of 4-tert-butylphenyl salicylate through down-regulation of the NF-kappa B pathway

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• 作者：Yun Hee Choi ; Baek Hee Na ; Yoon Seok Choi…
• 关键词：Anti ; inflammatory effect ; 4 ; tert ; Butylphenyl salicylate ; NF ; κB pathway ; COX ; 2 ; iNOS
• 刊名：Archives of Pharmacal Research
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：39
• 期：3
• 页码：429-436
• 全文大小：887 KB
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• 作者单位：Yun Hee Choi (1)
  Baek Hee Na (1)
  Yoon Seok Choi (1)
  Md. Saifur Rahman (1)
  Mi Ri Kim (1)
  Jun-Pil Jee (1)
  Jihoon Shin (2)
  Joo Won Suh (3)
  Jin Cheol Yoo (1)
  
  1. Department of Pharmacy, College of Pharmacy, Chosun University, Gwangju, 501-759, Korea
  2. Department of Complementary & Alternative Medicine, Chosun University, Gwangju, 501-759, Korea
  3. Center for Nutraceutical and Pharmaceutical Materials, Myongji University, Yongin-si, Gyeonggi-do, Korea
  
• 刊物主题：Pharmacy; Pharmacology/Toxicology;
• 出版者：Springer Netherlands
• ISSN：1976-3786

文摘

The salicylic acid derivative 4-tert-butylphenyl salicylate (4-TBPS) possesses anti-inflammatory activity. We demonstrated this and elucidated the mechanisms involved by using the lipopolysaccharide-stimulated Raw 264.7 mouse macrophage model. The 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, western blot, enzyme-linked immunosorbent assay, and reverse transcriptase-polymerase chain reaction were performed to explore 4-TBPS anti-inflammatory activity. We found that 4-TBPS decreased nitric oxide production without cytotoxic effects on macrophages and reduced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 in a dose-dependent manner. Additionally, mRNA expressions of iNOS and COX-2 significantly reduced, with concentrations between 1 and 15 µg/ml. Furthermore, 4-TBPS significantly inhibited the production of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin- (IL)-1β, and IL-6. Moreover, mRNA gene expression of TNF-α, IL-1β, and IL-6 was attenuated in a dose-dependent manner. 4-TBPS potently inhibited translocation of nuclear factor-κB (NF-κB) into the nucleus by degrading IκB kinase (IκBα) following its phosphorylation, thereby causing NF-κB to remain inactive. Collectively, our data indicate that 4-TBPS significantly (p < 0.01) targets the inflammatory response of macrophages via inhibition of iNOS, COX-2, TNF-α, IL-1β, and IL-6 through downregulation of the NF-κB pathway. This indicates that 4-TBPS may have therapeutic potential in inflammatory disorders.