ArticleBiomolecules & biomedicine2025
Jianpi Yiqi Busui prescription alleviates myasthenia gravis by regulating Th17 through the TAK1/P38 MAPK/eIF-4E signaling pathway.
Article in Biomolecules & biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Jianpi Yiqi Busui Prescription (JYBP), a traditional Chinese medicine formula (TCM), is used in the treatment of myasthenia gravis (MG). However, its mechanisms of action still require further clarification. In this study, an experimental autoimmune MG (EAMG) rat model was established for research. Changes in body weight, forelimb grip strength, Lennon clinical score, and antifatigue ability of EAMG model rats were recorded to evaluate the effectiveness of JYBP. Flow cytometry was utilized to count Th17, Th1, Th2, and Treg cells in lymphocytes. ELISA and RT-qPCR were used to measure acetylcholine receptor antibody (AChR-Ab) and Th17-related cytokines, including IL-17, IL-21, IL-23, TNF-α, TGF-β, IL-1β, and IL-6. Western blot and immunofluorescence staining were used to detect the expression levels of key proteins and their phosphorylated forms, such as transforming growth factor beta-activated kinase 1 (TAK1), P38 mitogen-activated protein kinase (P38 MAPK), and eukaryotic initiation factor 4E (eIF-4E). The results indicate that JYBP can increase the body weight of EAMG model rats, improve grip strength and antifatigue ability, and reduce the Lennon clinical score and AChR-Ab concentration. Mechanistic studies indicate that JYBP can inhibit the differentiation of CD4+ T cells into Th17 and Th1, promote their differentiation into Th2 and Treg, and regulate the expression of Th17-related cytokines. Further research shows that JYBP can reduce the expression of related proteins in the TAK1/P38 MAPK/eIF-4E signaling pathway. In conclusion, JYBP can alleviate the condition of EAMG model rats, positively affecting MG treatment. The inhibitory effect of JYBP on the differentiation of CD4+ T cells into Th17 may be related to the TAK1/P38 MAPK/eIF-4E signaling pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.