Evidence map›Paper›PMID 37551407›Full record

ArticleDrug design, development and therapy2023

Dioscin Ameliorates Experimental Autoimmune Thyroiditis via the mTOR and TLR4/NF-κB Signaling.

Chengfei Zhang, Qiue Zhang, Lingling Qin, Zhiyi Yan, Lili Wu, Tonghua Liu

Abstract read
In one paragraph

Article in Drug design, development and therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Revealing the Mechanism of Buzhong Yiqi Tang in Ameliorating Autoimmune ThyroiditisCombinatorial chemistry & high throughput screening · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Chengfei Zhang *School of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.ORCID 0000-0001-7390-1465
Qiue Zhang *School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.ORCID 0009-0004-9835-3951
Lingling Qin *Technology Department, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Zhiyi YanKey Laboratory of Health Cultivation of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, People's Republic of China.ORCID 0000-0001-9828-7705
Lili WuTechnology Department, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Tonghua LiuKey Laboratory of Health Cultivation of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, People's Republic of China.ORCID 0000-0001-7015-5348

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Autoimmune thyroiditis (AIT) is a common autoimmune disease that causes thyroid dysfunction. Clinical symptoms in Hashimoto thyroiditis patients were improved after oral administration of dioscin. However, the mechanisms involved in the therapeutic effect remain unclear. Methods: The protective effects and potential mechanisms of dioscin for autoimmune thyroiditis were explored in a rat model of thyroglobulin-induced autoimmune thyroiditis. Firstly, the rat model of AIT was obtained by subcutaneous injection of thyroglobulin and drinking the sodium iodide solution, followed by gavage administration for 8 weeks. Rats were sacrificed after anaesthesia, serum and thyroid samples were preserved. Serum triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyrotropin (TSH), thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb), and thyrotropin receptor antibody (TRAb) expressions were measured by enzyme-linked immunosorbent assay (ELISA). Morphological changes were observed by H&E staining. Next, we used transcriptomics techniques to find the potential therapeutic target of dioscin. Finally, we validated the transcriptomic results by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC-P), respectively. Results: Animal experiments showed that dioscin regulated T3, T4, FT3, TSH, TgAb, TPOAb, and TRAb and alleviated the pathological process in a dose-dependent manner, with the high-dose group showing optimal efficacy. In the transcriptome, the nuclear factor kappa B (NF-κB) pathway was identified by KEGG enrichment analysis and validated by RT-PCR and IHC-P. The relative expression of NF-κB, mechanistic target of rapamycin (mTOR), and toll-like receptor 4 (TLR4) mRNA and protein were decreased in the dioscin-treated group compared to the AIT model group. Conclusion: Our results suggest that dioscin treatment improved thyroid function and downregulated TGAb, TPOAb and TRAb levels in rat models of AIT, which may alleviate the pathological process and suppress the inflammatory response by inhibiting mTOR and TLR4/NF-κB pathways.

Indexed as

Hashimoto DiseaseThyroiditis, AutoimmuneAnimalsAutoantibodiesDiosgeninNF-kappa BRatsThyroglobulinThyrotropinThyroxineToll-Like Receptor 4TOR Serine-Threonine KinasesTriiodothyronineAutoantibodiesdioscinDiosgeninmTOR protein, ratNF-kappa BThyroglobulinThyrotropinThyroxineToll-Like Receptor 4TOR Serine-Threonine KinasesTriiodothyronineautoimmune thyroiditisdioscinTLR4/NF-κBtranscriptome

Identifiers

PMID37551407
PMCPMC10404412

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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.