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Astragalus Compound Eases Joint Damage in Mice With Arthritis

A compound from astragalus root reduced joint inflammation in arthritic mice by shifting gut bacteria and rebalancing two key immune cell types.

Dried herbal roots and slices in a wooden bowl beside glass cupping cups.
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A compound from astragalus root eased joint inflammation and bone damage in mice with rheumatoid arthritis, according to a mouse study published October 21, 2026 in Molecules.

42-daymouse study
100mg/kg/day dose

Researchers induced rheumatoid arthritis-like disease in male mice, then gave one group astragalus polysaccharide, a compound extracted from astragalus root, at 100 mg per kg daily for 42 days, either starting before or after joint disease set in. Compared with untreated arthritic mice, both astragalus groups had better bone volume on imaging and lower blood levels of two inflammation-driving proteins, TNF-α and IL-17, alongside higher levels of the anti-inflammatory signal IL-10. In spleen tissue, astragalus treatment lowered the share of Th17 cells, an inflammation-driving immune cell type, while raising Treg cells, shifting the Th17/Treg balance toward normal. Each group in the main experiment had 8 mice.

Researchers then transplanted gut bacteria from astragalus-treated mice into separate arthritic mice (5 per group). The recipients showed enrichment of several bacterial genera, including Ligilactobacillus, Lactobacillus, Limosilactobacillus and Bacteroides, which tracked with less joint inflammation and preserved bone structure.

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Gut bacteria transplanted from treated mice tracked with less joint inflammation and preserved bone in new arthritic mice, so the gut appears to be part of how the compound works. That fits the Th17 and Treg shift seen in the treated mice, since gut microbes are known to shape how these immune cells develop.

Astragalus Polysaccharide Dose in Arthritic Mice

Astragalus Polysaccharide Dose in Arthritic MiceMice with collagen-induced arthritis, treated daily for 42 days. 100 mg/kg/dayMice with collagen-induced arthritis, treated daily for 42days100 mg/kg/day
Molecules, 2026, Yao et al.

This is a mouse study using only male animals, with small comparison groups of 8 or 5 per group, so whether the same gut-immune pathway drives joint protection in people with rheumatoid arthritis is not yet shown. The authors note the study did not analyze which specific gut bacterial byproducts are responsible.

Dr. Axe’s Take

Rheumatoid arthritis is an autoimmune disease, and this mouse study adds to the evidence that gut bacteria deserve a bigger place in autoimmune care. Calming an overactive Th17 response while supporting the Treg cells that settle inflammation is exactly what I would expect from a gut-first approach. You do not need to wait for human astragalus trials to start caring for your gut if joint inflammation is a concern: eat fermented foods like sauerkraut and kefir, build meals around fiber-rich vegetables, and work in anti-inflammatory foods like turmeric, ginger and wild-caught salmon. Keep working with your doctor on any arthritis medication.

Dr. Axe— Dr. Axe

Study summary

Who
Male DBA/1 mice with collagen-induced arthritis; 8 mice per group in the main experiment, 5 per group in the fecal transplant experiment.
Design
Animal study; arthritic mice given astragalus polysaccharide prophylactically or therapeutically, compared with untreated and methotrexate-treated arthritic mice; separate fecal transplant experiment.
Dose
Astragalus polysaccharide, 100 mg/kg/day by gavage for 42 days; methotrexate comparison, 0.065 mg/kg weekly.
Primary result
Astragalus-treated mice had higher bone volume, lower blood TNF-α and IL-17, and higher IL-10 than untreated arthritic mice.
Secondary
Th17 cells decreased and Treg cells increased in spleen tissue, shifting the Th17/Treg ratio toward normal; fecal transplant from treated mice reduced joint inflammation and enriched gut bacteria including Ligilactobacillus, Lactobacillus, Limosilactobacillus and Bacteroides in recipient mice.
Funding / conflicts
Funders listed in the journal record: Natural Science Foundation of Chongqing; National Natural Science Foundation of China. Competing interests: The authors declare no conflicts of interest.
Date
Oct 21, 2026
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