1. Academic Validation
  2. Anti-Inflammatory Effects of Catalpalactone Isolated from Catalpa ovata in LPS-Induced RAW264.7 Cells

Anti-Inflammatory Effects of Catalpalactone Isolated from Catalpa ovata in LPS-Induced RAW264.7 Cells

  • Molecules. 2019 Mar 29;24(7):1236. doi: 10.3390/molecules24071236.
Hyo-Young Kim 1 Ah-Reum Han 2 Yun-Seo Kil 3 Eun Kyoung Seo 4 Chang Hyun Jin 5
Affiliations

Affiliations

  • 1 Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 56212, Korea. [email protected].
  • 2 Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 56212, Korea. [email protected].
  • 3 College of Pharmacy, Graduate School of Pharmaceutical Science, Ewha Womans University, Seoul 03760, Korea. [email protected].
  • 4 College of Pharmacy, Graduate School of Pharmaceutical Science, Ewha Womans University, Seoul 03760, Korea. [email protected].
  • 5 Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 56212, Korea. [email protected].
Abstract

Catalpa ovata (Bignoniaceae) is widely distributed throughout Korea, China, and Japan. This study investigated the anti-inflammatory effects of catalpalactone isolated from C. ovata in lipopolysaccharide (LPS)-induced RAW264.7 cells. Catalpalactone significantly inhibited nitric oxide (NO) production and inducible NO Synthase (iNOS) expression in LPS-induced RAW264.7 cells. The levels of cytokines such as interleukin-6 and tumor necrosis factor-α were reduced under catalpalactone exposure in LPS-induced RAW264.7 cells. Additionally, catalpalactone suppressed signal transducer and activator of transcription 1 (STAT-1) protein expression and interferon-β (IFN-β) production. Treatment with catalpalactone prevented interferon regulatory factor 3 (IRF3) and nuclear factor-κB (NF-κB) activation. Taken together, these results suggest that the anti-inflammatory effects of catalpalactone are associated with the suppression of NO production and iNOS expression through the inhibition of IRF3, NF-κB, and IFN-β/STAT-1 activation.

Keywords

Catalpa ovata; IRF3; NF-κB; catalpalactone; lipopolysaccharide.

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