ArticleJournal of inflammation research2023
Theaflavin-3,3'-Digallate Ameliorates Collagen-Induced Arthritis Through Regulation of Autophagy and Macrophage Polarization.
Article in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Advances regarding physiological functions and mechanisms of theaflavin‑3,3'‑digallate (Review).Molecular medicine reports · 2026Review
- Advances in traditional Chinese medicine for modulating macrophage polarization in the treatment of rheumatoid arthritis.Frontiers in pharmacology · 2026Review
- Theaflavin-3,3'-digallate triggers apoptosis in osteosarcoma cells via the caspase pathway.Journal of Cancer · 2025Article
- Inflammation preservation strategy: reconciling pain control and disc resorption in lumbar disc herniation.Frontiers in immunology · 2025Review
- LncRNA MIAT suppresses inflammation in LPS-induced J774A.1 macrophages by promoting autophagy through miR-30a-5p/SOCS1 axi.Scientific reports · 2024Article
- Machine learning and bioinformatics analysis to identify autophagy-related biomarkers in peripheral blood for rheumatoid arthritis.Frontiers in genetics · 2023Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Previous studies have presented that theaflavin-3,3'-digallate (TFDG), one of natural flavonoids, have protective effects on collagen-induced arthritis (CIA). Besides, it was reported that TFDG could affect inflammatory signaling pathways, like NF-κB, JNK, and so on, to ameliorate inflammation. However, the anti-inflammatory mechanisms mentioned above are common to natural flavonoid products including TFDG. Therefore, this study aimed to further investigate the other mechanisms of TFDG against CIA. Methods: DBA/1 mice (8-10 weeks) were intravenously injected Freund's Adjuvant (100μL) at the base of tail and intraperitoneally injected PBS or different dosage of TFDG (1 mg/kg or 10 mg/kg). Then the paw and knee tissues were collected to assess the severity of joint destruction. In vitro experiments, bone marrow macrophages (BMMs) were exposed to TNF-α (10ng/mL) with or without different concentrations of TFDG (0.1μmol/L or 1.0μmol/L). Besides, the targets of TFDG were predicted with docking software and were verified through experiment. Results: TFDG treatment could reduce M1 macrophage (pro-inflammatory) and inflammatory cytokines, such as IL-1, IL- 6 and TNF-α, both in vitro and in vivo. At the same time, the M2 macrophage (alternatively activated) polarization was promoted by TFDG. Animal experiments showed TFDG ameliorated joint destructions. For investigating the mechanisms, the targets of TFDG were predicted by bioinformatics tools. According to predictions, we hypothesized that TFDG could act with BCL-2 to weaken the interaction between BCL-2 and Beclin1. Beclin1 plays a central role in autophagy, and we found that the autophagy level of BMMs was recovered by TFDG. Besides, 3-MA, an autophagy inhibitor, could attenuate the therapeutic effect of TFDG. Conclusion: TFDG protected against collagen-induced arthritis by attenuating the inflammation and promoting anti-inflammatory M2 macrophage polarization through controlling autophagy.
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