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热处理人参皂苷对一氧化氮合酶的诱导作用。

Induction of nitric oxide synthase by saponins of heat-processed ginseng.

作者信息

Kim Ji Yeon, Lee Hwa Jin, Kim Ji Sun, Ryu Jae-Ha

机构信息

College of Pharmacy, Sookmyung Women's University, Seoul, Korea.

出版信息

Biosci Biotechnol Biochem. 2005 May;69(5):891-5. doi: 10.1271/bbb.69.891.

Abstract

Total saponin of heat-processed ginseng (TSHG) stimulated the production of nitric oxide (NO) in interferon-gamma (IFN-gamma)-primed macrophages through the increased expression of inducible nitric oxide synthase (iNOS). However, TSHG by itself had a very weak effect on the NO synthesis without IFN-gamma priming. The saponins of white ginseng inhibited the NO production in lipopolysaccharide (LPS)/IFN-gamma activated macrophages rather than the stimulation of NO production found in IFN-gamma primed macrophages. The NO production by TSHG-stimulated macrophages was inhibited by the NOS inhibitor (N(G)-monomethyl-L-arginine (L-NMMA)) and nuclear factor-kappaB inhibitor (pyrrolidine dithiocarbamate (PDTC)). TSHG showed different serum-dependence from LPS on the activation of IFN-gamma primed macrophages. This property of TSHG may explain the intensified anti-tumor properties of heat-processed ginseng through its immunostimulating activity.

摘要

炮制人参总皂苷(TSHG)通过增加诱导型一氧化氮合酶(iNOS)的表达,刺激经γ-干扰素(IFN-γ)预处理的巨噬细胞产生一氧化氮(NO)。然而,TSHG本身对未经IFN-γ预处理的巨噬细胞的NO合成作用非常微弱。白参皂苷抑制脂多糖(LPS)/IFN-γ激活的巨噬细胞产生NO,而不是像在经IFN-γ预处理的巨噬细胞中那样刺激NO产生。TSHG刺激的巨噬细胞产生的NO被一氧化氮合酶抑制剂(N(G)-单甲基-L-精氨酸(L-NMMA))和核因子-κB抑制剂(吡咯烷二硫代氨基甲酸盐(PDTC))抑制。在激活经IFN-γ预处理的巨噬细胞方面,TSHG显示出与LPS不同的血清依赖性。TSHG的这一特性可能解释了炮制人参通过其免疫刺激活性增强的抗肿瘤特性。

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