ArticleChinese medicine2024
Formononetin reverses Treg/Th17 imbalance in immune-mediated bone marrow failure mice by regulating the PI3K/Akt signaling pathway.
Article in Chinese medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 12 citations in OpenAlex.
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- Black Phosphorus Nanomaterials and the Senescent Osteoimmune Microenvironment: Mechanisms, Opportunities, Challenges, and Future Outlook.International journal of nanomedicine · 2026Review
- Formononetin derived from Parabacteroides merdae alleviates MPTP-induced Parkinson's disease in mice by inhibiting ferroptosis via the PI3K-AKT-ferritinophagy axis.Communications biology · 2025Article
- A Case of Severe Anemia in Pregnancy Treated With Traditional Chinese Medicine.Clinical case reports · 2025Article
- Advances in synthesizing plant-derived isoflavones and their precursors with multiple pharmacological activities using engineered yeasts.Microbial cell factories · 2025Review
- Umbilical Cord Mesenchymal Stem Cell-Derived Extracellular Nanovesicles Alleviated Colitis via Modulating Th17/Treg Balance Through Hsa-miR-27b-3p-Mediated Suppression of PI3K/AKT/STAT3 Signaling Pathway.International journal of nanomedicine · 2025Article
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6 authors at 4 institutions in 1 country.
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Abstract
backgroundSevere aplastic anemia (SAA) is a syndrome of bone marrow failure which is life-threatening. Recent studies have demonstrated that CD4 + T cell subsets, including T regulatory (Treg) and T helper 17 (Th17) cells, play a pivotal role in the pathogenesis of SAA. Formononetin (FMN) is a natural compound extracted from the traditional Chinese medicine Huangqi, which has the ability to regulate the imbalance of Treg/Th17 cells in some inflammatory diseases. Nevertheless, the therapeutic effect of FMN in SAA has yet to be definitively established. Therefore, the objective of this research was to investigate the effect of FMN on SAA and elucidate its underlying mechanism.
methodsIn vivo experiments, the mice were divided into the following five groups: control, model, low-dose FMN, high-dose FMN, and positive control cyclosporine A group. The immune-mediated bone marrow failure (BMF) mouse model was established by the total body X-ray radiation and lymphocyte infusion. After 10 days of continuous administration of FMN, the numbers of Treg/Th17 cells in the bone marrow and spleen were assessed by flow cytometry. The protein expressions of PI3K/Akt pathway in the bone marrow and spleen was assessed by immunohistochemistry and western blotting. In vitro, the impact of FMN on the differentiation of naive CD4 + T cells into Treg cells was investigated by flow cytometry and ELISA.
resultsIn comparison with the control group, the model group showed a reduction in bone marrow nucleated cells, a significant decrease in peripheral blood cells, and an altered CD8 + /CD4 + T cell ratio. These findings indicate the successful establishment of a mouse model of immune-mediated BMF. After FMN treatment, there were the increased levels of red blood cells and hemoglobin. In addition, FMN mitigated the bone marrow destruction and restored the CD8 + /CD4 + T cell ratio. Furthermore, in comparison with the control group, the model group showed the decreased levels of Treg cells and the increased levels of Th17 cells. After FMN treatment, there was a significantly increased number of Treg cells and a decreased number of Th17 cells. Additionally, FMN remarkably down-regulated the expression levels of PI3K and Akt proteins in immune-mediated BMF mice.
conclusionsFMN alleviates immune-mediated BMF by modulating the balance of Treg/Th17 cells through the PI3K/Akt signaling pathway.
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