Anti-inflammatory potential of peat moss extracts in lipopolysaccharide-stimulated RAW 264.7 macrophagesopen access
- Authors
- Choi, Woo-Suk; Jeong, Jin-Woo; Kim, Sung Ok; Kim, Gi-Young; Kim, Byung-Woo; Kim, Cheol Min; Seo, Yong-Bae; Kim, Woe-Yeon; Lee, Sang-Yeol; Jo, Kwon-Ho; Choi, Young Ju; Choi, Yung Hyun; Kim, Gun-Do
- Issue Date
- Oct-2014
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- peat moss; anti-inflammation; nuclear factor-kappa B; mitogen-activated protein kinase; nuclear factor-like 2/heme oxygenase-1
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.34, no.4, pp.1101 - 1109
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
- Volume
- 34
- Number
- 4
- Start Page
- 1101
- End Page
- 1109
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/18727
- DOI
- 10.3892/ijmm.2014.1881
- ISSN
- 1107-3756
- Abstract
- The aim of the present study was to identify the anti-inflammatory and anti-oxidative effects of peat moss aqueous extract (PME) on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. To demonstrate the anti-inflammatory and antioxidant effects of PME, the levels of nitric oxide (NO) and cytokines were measured using Griess reagent and cytokine ELISA kits, respectively. Reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot analysis were conducted to evaluate the expression of genes and proteins. Immunofluorescence was used to measure the expression and translocation of transcription factors. Pre-treatment with PME inhibited the production of prostaglandin E-2 and NO by suppressing the gene expression of cyclooxygenase-2 and inducible NO synthase, respectively. The LPS-stimulated gene expression and the production of tumor necrosis factor-alpha and interleukin-1 beta were significantly reduced by PME. In the LPS-stimulated RAW 264.7 cells, nuclear factor-kappa B (NF-kappa B) translocated from the cytosol to the nucleus, while pre-treatment with PME induced the sequestration of NF-kappa B in the cytosol through the inhibition of I kappa B alpha degradation. In the same manner, PME contributed to the inhibition of the activation of mitogen-activated protein kinases. In addition, the PME-treated RAW 264.7 cells facilitated the activation of nuclear factor-like 2 (Nrf2), and in turn, enhanced heme oxygenase-1 (HO-1) expression. These results indicate that PME exerts anti-inflammatory and antioxidant effects, and suggest that PME may neutralize inflammation and prevent cellular damage by oxidative stress.
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