ArticleCombinatorial chemistry & high throughput screening2026
Astragalosides Promote MH7A Cell Apoptosis by Suppressing WTAP-mediated m6A Methylation of TRAIL-DR4.
Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Rewiring immunity in rheumatoid arthritis: metabolic and epigenetic therapeutic strategies.Frontiers in pharmacology · 2026Review
- The PANoptotic mosaic of rheumatoid arthritis: epitranscriptomic regulation, systemic relays, and precision death-mode editing.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundAstragaloside (AST), a natural saponin extracted from Astragalus membranaceus (Fisch.) Bunge., has been consistently utilized in the treatment of rheumatoid arthritis (RA). N6-methyladenosine (m6A), the most prevalent modification of mRNA, is associated with the progression of various diseases, including RA. Nonetheless, the effects of AST on m6A modification in RA remain to be elucidated.
methodsThe MH7A cell model was established through induction with TNF-α. The effects of AST on the expression levels of WTAP, BAX, BCL2, and TRAIL-DR4 were evaluated utilizing immunofluorescence, RT-qPCR, and Western blot analysis. Furthermore, CCK-8 and flow cytometry were used to assess MH7A cell viability, cell cycle, apoptosis, and proliferation. Then, the m6A modification of TRAIL-DR4 was elucidated via MeRIP-qPCR.
resultsThe optimal dose administration time was 50 μg/mL at 48 h. AST not only reduced the expression levels of WTAP, BCL2, BAX, TRAIL-DR4, and the m6A modification level of TRAIL-DR4 but also significantly enhanced apoptosis in MH7A cell, while inhibiting cell viability and proliferation. Furthermore, AST was capable of reversing the effect on MH7A cell proliferation and apoptosis induced by WTAP overexpression.
conclusionThis study elucidates the protective role of AST on MH7A cells by attenuating m6A/WTAP-mediated apoptosis, offering novel insights into the mechanisms of AST.
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Registered trials
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