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果糖精氨酸,一种高丽红参的非皂苷分子,可减弱AIM2炎性小体的激活。

Fructose-arginine, a non-saponin molecule of Korean Red Ginseng, attenuates AIM2 inflammasome activation.

作者信息

Ahn Huijeong, Han Byung-Cheol, Lee Seung-Ho, Lee Geun-Shik

机构信息

College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University, Chuncheon, Republic of Korea.

Korea Ginseng Research Institute, Korea Ginseng Corporation, Daejeon, Republic of Korea.

出版信息

J Ginseng Res. 2020 Nov;44(6):808-814. doi: 10.1016/j.jgr.2020.06.002. Epub 2020 Jul 21.

DOI:10.1016/j.jgr.2020.06.002
PMID:33192124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7655492/
Abstract

BACKGROUND

Korean Red Ginseng extract (RGE) has been reported to act as an inflammasome modulator. Ginsenosides, saponin molecules of RGE, selectively inhibit activation of NLRP3 and AIM2 inflammasomes, while non-saponin molecules of RGE upregulate inflammasome components associated with the initiation of NLRP3 inflammasome activation. In this study, we investigated the effect of non-saponin components of RGE on AIM2 inflammasome activation.

METHODS

The role of non-saponins of RGE on AIM2 inflammasomes was tested in mouse bone marrow-derived macrophages, a human monocyte-like cell line, and a mouse animal model. Cells or mice were transfected with dsDNA or inoculated with to activate AIM2 inflammasomes. Several indices of inflammasome activation were examined via immunoblot or ELISA analysis.

RESULTS

The non-saponin fraction and saponin-eliminating fraction (SEF) of RGE selectively attenuated the activation of AIM2 inflammasomes, but not that of NLRP3 or NLRC4 inflammasomes. Fructose-arginine, an amino-sugar, was shown to be effective against AIM2 inflammasome activation.

CONCLUSION

Non-saponins of RGE, such as fructose-arginine, might be effective in regulating infectious and autoimmune diseases resulting from AIM2 inflammasome activation.

摘要

背景

据报道,韩国红参提取物(RGE)可作为一种炎性小体调节剂。人参皂苷是RGE的皂苷分子,可选择性抑制NLRP3和AIM2炎性小体的激活,而RGE的非皂苷分子则上调与NLRP3炎性小体激活起始相关的炎性小体成分。在本研究中,我们研究了RGE的非皂苷成分对AIM2炎性小体激活的影响。

方法

在小鼠骨髓来源的巨噬细胞、人单核细胞样细胞系和小鼠动物模型中测试了RGE非皂苷对AIM2炎性小体的作用。用双链DNA转染细胞或小鼠,或接种以激活AIM2炎性小体。通过免疫印迹或ELISA分析检测炎性小体激活的几个指标。

结果

RGE的非皂苷组分和去皂苷组分(SEF)选择性减弱AIM2炎性小体的激活,但不影响NLRP3或NLRC4炎性小体的激活。氨基糖果糖精氨酸被证明对AIM2炎性小体激活有效。

结论

RGE的非皂苷,如果糖精氨酸,可能对调节由AIM2炎性小体激活引起的感染性和自身免疫性疾病有效。

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