Anti-inflammatory properties of samidin from Seseli resinosum through suppression of NF-κB and AP-1-mediated-genes in LPS-stimulated RAW 264.7 cells

Khan S., Shehzad O., Lee K. J., Tosun A., Kim Y. S.

Archives of Pharmacal Research, cilt.37, sa.11, ss.1496-1503, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 37 Sayı: 11
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1007/s12272-014-0346-0
  • Dergi Adı: Archives of Pharmacal Research
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1496-1503
  • Anahtar Kelimeler: Seseli resinosum, Samidin, Inflammation, NF-kappa B, AP-1, LPS, NITRIC-OXIDE, CHRONIC INFLAMMATION, TNF-ALPHA, INHIBITION, MACROPHAGES, TURKEY, EXPRESSION, COUMARINS, MECHANISM, PATHWAYS
  • Ankara Üniversitesi Adresli: Evet

Özet

© 2014 The Pharmaceutical Society of Korea.Seseli is a herb widely used for its anti-inflammation, anti-flatulence and various other healing properties. In the present study, we investigated the effects of samidin on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The results demonstrated that samidin significantly inhibited the production of nitric oxide, as well as the gene expression levels of inducible nitric oxide synthase and cyclooxygenase-2. The results from an electrophoretic mobility shift assay illustrated that samidin significantly suppressed NF-κB and AP-1 DNA-binding affinity. In addition, both the NF-κB subunit p65 and the AP-1-related c-jun were markedly inhibited by samidin. The time course experiment demonstrated that samidin showed significant inhibitory effect on p38 and JNK activation. Furthermore, tumor necrosis factor-α mRNA level were remarkably down-regulated by samidin in LPS-stimulated macrophages based on quantitative-real-time polymerase chain reaction. Our results suggested that samidin has a potential to be developed as a therapeutic agent for various inflammatory diseases.