Astragalus Polysaccharides Alleviate Inflammatory Damage in Murine Rheumatoid Arthritis by Modulating Th17/Treg Balance via the Gut–Joint Axis
- 1Department of Pharmacy, The First Affiliated Hospital (Southwest Hospital) of Third Military Medical University (Army Medical University), Chongqing 400038, China
- 2Department of Vascular and Endovascular Surgery, The First Affiliated Hospital (Southwest Hospital) of Army Medical University, Chongqing 400038, China
- 3Department of Dermatology, The First Affiliated Hospital (Southwest Hospital) of Army Medical University, Chongqing 400038, China
Abstract
Astragalus polysaccharides (APSs) have demonstrated protective effects in RA models; however, the underlying microbe–host crosstalk remains unclear. In this study, collagen-induced arthritis (CIA) was established in mice, followed by prophylactic and therapeutic APS administration. The following were then assessed: articular histopathology, splenic Th17/Treg frequencies via flow cytometry, serum and joint cytokine profiles via ELISA and immunohistochemistry, gut microbial metagenomes, and bone erosion via Safranin O–fast green staining. It was found that APS treatment significantly attenuated joint inflammation and bone destruction, rebalanced the Th17/Treg ratio, and reduced pro-inflammatory cytokines (TNF-α and IL-17) while elevating anti-inflammatory IL-10 both systemically and locally. Subsequently, fecal microbiota from APS-treated donor mice was transplanted via oral gavage into CIA recipient mice. APS reversed RA-associated gut dysbiosis by enriching Ligilactobacillus, Lactobacillus, Limosilactobacillus, and Bacteroides, and these microbial shifts closely paralleled diminished articular inflammation and preserved bone architecture. Collectively, these findings indicate that APS mitigates RA progression by reconfiguring the gut microbial ecosystem—favoring beneficial taxa while curbing pathobionts—thereby restoring intestinal homeostasis, normalizing the Th17/Treg axis, and suppressing systemic and articular inflammatory responses.
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BibTeX
@article{yao2026astragalus,
title = {{Astragalus Polysaccharides Alleviate Inflammatory Damage in Murine Rheumatoid Arthritis by Modulating Th17/Treg Balance via the Gut–Joint Axis}},
author = {Pu Yao and Jing Huang and Wenying Liu and Qian Yuan and Jun Lv},
journal = {Molecules},
year = {2026},
month = oct,
doi = {10.3390/molecules31203788},
url = {https://www.mdpi.com/1420-3049/31/20/3788},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Astragalus Polysaccharides Alleviate Inflammatory Damage in Murine Rheumatoid Arthritis by Modulating Th17/Treg Balance via the Gut–Joint Axis
AU - Pu Yao
AU - Jing Huang
AU - Wenying Liu
AU - Qian Yuan
AU - Jun Lv
PY - 2026
DA - 2026/10/01
JO - Molecules
DO - 10.3390/molecules31203788
UR - https://www.mdpi.com/1420-3049/31/20/3788
AB - Astragalus polysaccharides (APSs) have demonstrated protective effects in RA models; however, the underlying microbe–host crosstalk remains unclear. In this study, collagen-induced arthritis (CIA) was established in mice, followed by prophylactic and therapeutic APS administration. The following were then assessed: articular histopathology, splenic Th17/Treg frequencies via flow cytometry, serum and joint cytokine profiles via ELISA and immunohistochemistry, gut microbial metagenomes, and bone erosion via Safranin O–fast green staining. It was found that APS treatment significantly attenuated joint inflammation and bone destruction, rebalanced the Th17/Treg ratio, and reduced pro-inflammatory cytokines (TNF-α and IL-17) while elevating anti-inflammatory IL-10 both systemically and locally. Subsequently, fecal microbiota from APS-treated donor mice was transplanted via oral gavage into CIA recipient mice. APS reversed RA-associated gut dysbiosis by enriching Ligilactobacillus, Lactobacillus, Limosilactobacillus, and Bacteroides, and these microbial shifts closely paralleled diminished articular inflammation and preserved bone architecture. Collectively, these findings indicate that APS mitigates RA progression by reconfiguring the gut microbial ecosystem—favoring beneficial taxa while curbing pathobionts—thereby restoring intestinal homeostasis, normalizing the Th17/Treg axis, and suppressing systemic and articular inflammatory responses.
SN - 1420-3049
ER -