대식세포의 NO, TNF-α 및 IL-1 생산에 미치는 상백피의 억제 효과

• 영문명: The suppressive effects of cortex mori on NO, TNF-α and IL-1 production by macrophage
• 발행기관: 한국예방수의학회
• 저자명: 윤창용(Chang Yong Yoon) 신동환(Dong Hwan Shin) 홍충만(Choong Man Hong) 이원규(Won Kyu Lee) 장동덕(Dong Deuk Jang) 조재천(Jae Chon Cho) 안재규(Jae Kyu Ahn) 안덕균(Deuk Kyun Ahn) 이무삼(Moo Sam Lee)
• 간행물 정보: 『Korean Journal of Veterinary Public Health』Vol.22, No.3, 281~292쪽, 전체 12쪽
• 주제분류: 의약학 > 면역학
• 파일형태: PDF
• 발행일자: 1998.09.30

영문 초록

Cortex Mori (Morus loba L., CM), the root bark of mulberry tree has heen used as an antiphlogistic, diuretic and expectorant in herval medicine. Recently, a few papers reported that phenolic extract of CM has hypotensive, hypoglycemic, antiviral and anticancer effects, and hot water extract of CM inhibitory effect on the degranulation and histamine release from activated mast cells. These previous studies suggest that CM has an antidotal activity against inflammation which was mediated mainly by macrophage-secreting inflammatory factors. This study was performed to evaluate the influences of CM on carrageenan-induced edema in vivo and release of inflammatory mediators such as NO(nitric oxide), TNF(tumor necrosis factor) and IL-1(interleukin-1) by macrophages stimulated with LPS(lipopolysaccharide) or IFN-γ(inteferon-γ) in vitro. Subcutaneous injections of carrageenan into the mouse paw rapidly induced local edema by increasing vascular permeability, but single intraperitoneal injection of CM extract at 30 minutes before carrageenan suppressed the development of edema. NO-and TNF production from macrophage stimulated by LPS or INF-γ were significantly suppressed, especially TNF secretion by up to 3~4 folds. LPS stimulated IL-1 production was also inhibited, but not significantly. Cell viability assay verified that the inhibition was not due to general cell toxicity. The results suggest that anti-inflammatory effects of CM results from inhibition of NO, TNF, and IL-1 production in inflammation associated-diseases.

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키워드

Cortex Mori Macrophage Nitric oxide TNF-a IL-1