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- Title
Alpinia katsumadai H Seed Extract Inhibit LPS-Induced Inflammation by Induction of Heme Oxygenase-1 in RAW264.7 Cells.
- Authors
Lee, Mee-Young; Seo, Chang-Seob; Lee, Jin-Ah; Shin, In-Sik; Kim, Su-Jeong; Ha, HeyKyung; Shin, Hyeun-Kyoo
- Abstract
In the present study, we investigated the effects of Alpinia katsumadai H (Zingiberaceae) seed ethanolic extract (AKEE) and its three components on the production of inflammatory mediators and some potential underlying mechanisms in lipopolysaccharide (LPS)-induced inflammation RAW264.7 cells. The whole formula, AKEE, and three major component compounds were then evaluated for their effects on inflammation-related parameters using LPS-induced RAW264.7 cells. Production of namely nitric oxide (NO) and cytokine levels were measured by the Griess reagent and ELISA, respectively. To investigate the underlying mechanisms of anti-inflammatory activities of AKEE, protein expression of nitric oxide synthase (inducible nitric oxide synthase, iNOS), heme oxygenase-1 (HO-1), and nuclear factor-kappa B (NF-κB) were evaluated by western blot analysis. AKEE and the major group of compounds in AKEE (alpinetin, cardamonin, and pinocembrin) complement exert anti-inflammatory effects for NO and PGE production. In addition, AKEE treatment significantly inhibited the LPS-induced production of interleukin-6 and tumor necrosis factor (TNF)-α, as well as the expression of iNOS. AKEE also induced HO-1 expression in RAW264.7 cells and inhibited the nuclear translocation of NF-κB by preventing degradation of the inhibitor kappa B-alpha. We also demonstrated that the effects of AKEE on TNF-α production were partially reversed by the HO-1 inhibitor tin protoporphyrin. These results indicate that AKEE and its major component may have anti-inflammatory activity via induction of HO-1 expression was partly responsible for the anti-inflammatory effects.
- Subjects
LIPOPOLYSACCHARIDES; INFLAMMATION; HEME oxygenase; ZINGIBERACEAE; NITRIC oxide; CYTOKINES; WESTERN immunoblotting; PLANT extracts
- Publication
Inflammation, 2012, Vol 35, Issue 2, p746
- ISSN
0360-3997
- Publication type
Article
- DOI
10.1007/s10753-011-9370-0