Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages

  • Authors:
    • Young-Chang Cho
    • Ye Rang Kim
    • Ba Reum Kim
    • Tran The Bach
    • Sayeon Cho
  • View Affiliations

  • Published online on: September 21, 2016     https://doi.org/10.3892/ijmm.2016.2746
  • Pages: 1596-1604
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Thunbergia alata (Acanthaceae) has been used traditionally to treat various inflammatory diseases such as fever, cough and diarrhea in East African countries including Uganda and Kenya. However, systemic studies elucidating the anti-inflammatory effects and precise mechanisms of action of T. alata have not been conducted, to the best of our knowledge. To address these concerns, we explored the anti-inflammatory effects of a methanol extract of T. alata (MTA) in macrophages. Non-cytotoxic concentrations of MTA (≤300 µg/ml) inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)‑stimulated RAW 264.7 macrophages by transcriptional regulation of inducible NO synthase in a dose-dependent manner. The expression of cyclooxygenase-2, the enzyme responsible for the production of prostaglandin E2, was unchanged by MTA at the mRNA and protein levels. MTA treatment inhibited interleukin (IL)-6 production and decreased the mRNA expression of pro‑inflammatory cytokines, including IL-6 and IL-1β. Tumor necrosis factor-α production and mRNA expression were not regulated by MTA treatment. The decreased production of inflammatory mediators by MTA was followed by the reduced phosphorylation of extracellular signal‑regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3). MTA treatment had no effect on activity of other mitogen‑activated protein kinases (MAPKs), p38, c-Jun N-terminal kinase (JNK), and nuclear factor-κB (NF-κB). These results indicate that MTA selectively inhibits the excessive production of inflammatory mediators in LPS-stimulated murine macrophages by reducing the activity of ERK and STAT3, suggesting that MTA plays an important inhibitory role in the modulation of severe inflammation.
View Figures
View References

Related Articles

Journal Cover

November-2016
Volume 38 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Cho Y, Kim YR, Kim BR, Bach TT and Cho S: Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages. Int J Mol Med 38: 1596-1604, 2016
APA
Cho, Y., Kim, Y.R., Kim, B.R., Bach, T.T., & Cho, S. (2016). Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages. International Journal of Molecular Medicine, 38, 1596-1604. https://doi.org/10.3892/ijmm.2016.2746
MLA
Cho, Y., Kim, Y. R., Kim, B. R., Bach, T. T., Cho, S."Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages". International Journal of Molecular Medicine 38.5 (2016): 1596-1604.
Chicago
Cho, Y., Kim, Y. R., Kim, B. R., Bach, T. T., Cho, S."Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages". International Journal of Molecular Medicine 38, no. 5 (2016): 1596-1604. https://doi.org/10.3892/ijmm.2016.2746