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黄芪多糖对法氏囊中chTLR4通路的激活作用。

chTLR4 pathway activation by Astragalus polysaccharide in bursa of Fabricius.

作者信息

Zhang Ruili, Yu Qun, Shi Guangliang, Liu Rui, Zhang Weiqian, Zhao Xia, Li Guangxing, Ge Ming

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

Harbin Veterinary Research Institute, Chinese Academy Agricultural Sciences, Harbin, 150001, China.

出版信息

BMC Vet Res. 2017 May 2;13(1):119. doi: 10.1186/s12917-017-1039-y.

DOI:10.1186/s12917-017-1039-y
PMID:28464901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5414374/
Abstract

BACKGROUND

The Toll-like receptor 4 (TLR4) pathway involves in the pathogen recognition and defense against infection in mammals. Considering that avian and mammalian TLR are differentially mediated, the action of a natural product on avian TLR4 pathway was unclear. High, medium and low doses of Astragalus polysaccharide (APS), were treated the chicken at 7-days-old age by gavage. The sIgA level in the intestinal fluid, the expression of chTLR4 mRNA/protein in bursa of Fabricius as well as the expression of downstream molecules of chTLR4 (chMyD88, chTRIF, chNF-κB, chIRF3, chIFN-β and chTNF-α) were measured on alternate days.

RESULTS

The content of sIgA and the chTLR4 mRNA expression/protein level were increased in non-dose-dependent manner after APS supplement. Also, the expressions of a subset of MyD88-independent pathway genes were more than MyD88-independent, in particular with low doses of APS supplement for 7 days.

CONCLUSIONS

These suggest that administration of APS activates chTLR4 pathway in bursa of Fabricius in MyD88-independent pathway. Meanwhile, low dose of APS shows better performance regarding the activation of chTLR4 and regulation of MyD88-independent pathway.

摘要

背景

Toll样受体4(TLR4)通路参与哺乳动物病原体识别及抗感染防御。鉴于禽类和哺乳动物的TLR介导方式存在差异,一种天然产物对禽类TLR4通路的作用尚不清楚。将高、中、低剂量的黄芪多糖(APS)于雏鸡7日龄时通过灌胃进行处理。每隔一天检测肠道液中sIgA水平、法氏囊中chTLR4 mRNA/蛋白表达以及chTLR4下游分子(chMyD88、chTRIF、chNF-κB、chIRF3、chIFN-β和chTNF-α)的表达。

结果

补充APS后,sIgA含量以及chTLR4 mRNA表达/蛋白水平呈非剂量依赖性增加。此外,MyD88非依赖途径的一部分基因的表达高于MyD88依赖途径,尤其是低剂量APS补充7天时。

结论

这些结果表明,给予APS可通过MyD88非依赖途径激活法氏囊中chTLR4通路。同时,低剂量APS在激活chTLR4和调节MyD88非依赖途径方面表现更佳。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ff6/5414374/9de8e479dec2/12917_2017_1039_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ff6/5414374/65ccd26fb8f3/12917_2017_1039_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ff6/5414374/f365299993e0/12917_2017_1039_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ff6/5414374/9de8e479dec2/12917_2017_1039_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ff6/5414374/65ccd26fb8f3/12917_2017_1039_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ff6/5414374/f365299993e0/12917_2017_1039_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ff6/5414374/9de8e479dec2/12917_2017_1039_Fig3_HTML.jpg

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