Anti-inflammatory Effects of Ethanolic Extract from Sargassum horneri (Turner) C. Agardh on Lipopolysaccharide-Simulated Macrophage Activation via NF-κB Pathway Regulation

被引:46
作者
Kim, Mi Eun [1 ]
Jung, Yun Chan [2 ,4 ]
Jung, Inae [1 ]
Lee, Hee-Woo [2 ]
Youn, Hwa-Young [2 ]
Lee, Jun Sik [1 ,3 ]
机构
[1] Chosun Univ, Dept Biol, Plus Res Team Bioact Control Technol BK21, Immunol Res Lab,Coll Nat Sci, Kwangju 501759, South Korea
[2] Seoul Natl Univ, Dept Vet Internal Med, Coll Vet Med, Seoul, South Korea
[3] Chosun Univ, Marine Biotechnol Res Ctr, Kwangju 501759, South Korea
[4] KPC Corp, Gwangju Si, Gyeonggi Do, South Korea
关键词
ESH; inflammation; macrophage; NF-kappa B; Sargassum horneri (Turner) C. Agardh; NITRIC-OXIDE PRODUCTION; RAW; 264.7; MACROPHAGES; SULFATED POLYSACCHARIDE; INFLAMMATION; MAPK; CYCLOOXYGENASE-2; DIFFERENTIATION; EXPRESSION; INDUCTION; FULVELLUM;
D O I
10.3109/08820139.2014.942459
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammation is major symptom of the innate immune response by infection of microbes. Macrophages, one of immune response related cells, play a role in inflammatory response. Recent studies reported that various natural products can regulate the activation of immune cells such as macrophage. Sargassum horneri (Turner) C. Agardh is one of brown algae. Recently, various seaweeds including brown algae have antioxidant and anti-inflammatory effects. However, anti-inflammatory effects of Sargassum horneri (Turner) C. Agardh are still unknown. In this study, we investigated anti-inflammatory effects of ethanolic extract of Sargassum horneri (Turner) C. Agardh (ESH) on RAW 264.7 murine macrophage cell line. The ESH was extracted from dried Sargassum horneri (Turner) C. Agardh with 70% ethanol and then lyophilized at -40 degrees C. ESH was not cytotoxic to RAW 264.7, and nitric oxide (NO) production induced by LPS-stimulated macrophage activation was significantly decreased by the addition of 200 mg/mL of ESH. Moreover, ESH treatment reduced mRNA level of cytokines, including IL-1 beta, and pro-inflammatory genes such as iNOS and COX-2 in LPS-stimulated macrophage activation in a dose-dependent manner. ESH was found to elicit anti-inflammatory effects by inhibiting ERK, p-p38 and NF-kappa B phosphorylation. In addition, ESH inhibited the release of IL-1b in LPS-stimulated macrophages. These results suggest that ESH elicits anti-inflammatory effects on LPS-stimulated macrophage activation via the inhibition of ERK, p-p38, NF-kappa B, and pro-inflammatory gene expression.
引用
收藏
页码:137 / 146
页数:10
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