ArticleInternational journal of medical sciences2022
SJMHE1 protects against excessive iodine-induced pyroptosis in human thyroid follicular epithelial cells through a toll-like receptor 2-dependent pathway.
Article in International journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Modulation of NF-κB and TLR Signaling Pathways and Complement Components in Ovine Maternal Thyroid During Early Pregnancy.International journal of molecular sciences · 2026Article
- Schistosoma japonicum peptide SJMHE1 promotes peripheral nerve regeneration via macrophage migrasome-derived miR-26b-5p targeting the PTEN/AKT axis.Journal of translational medicine · 2025Article
- Elucidating the role of Pyroptosis in papillary thyroid cancer: prognostic, immunological, and therapeutic perspectives.Cancer cell international · 2024Article
- Giardia VSPAS7 protein attenuates Giardia intestinalis-induced host macrophage pyroptosis.Parasites & vectors · 2023Article
- HMGB1 and Toll-like receptors: potential therapeutic targets in autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
To elucidate the effect of Schistosoma japonicum peptide (SJMHE1) on pyroptosis in thyroid follicular epithelial cells (TFCs) induced by excessive iodine and the potential mechanism, the effects of SJMHE1 were investigated in NaI-treated Nthy-ori 3-1 cells; and the involvement of the ROS/MAPK/NF-κB signaling pathways in these effects was evaluated by employing CCK-8 assays, flow cytometry, ELISA, and Western blotting experiments. We found that SJMHE1 significantly reduced NLRP3, N-terminus of gasdermin D (GSDMD-N) and cleaved caspase-1 (C-caspase-1) expression, and decreased IL-1β secretion in TFCs. SJMHE1 also markedly reduced reactive oxygen species (ROS) production, and decreased the phosphorylation levels of MAPK and NF-κB pathway members. Moreover, blocking of the Toll-like receptor 2 significantly impaired SJMHE1-mediated protection from excessive iodine-induced pyroptosis in TFCs. Therefore, our results suggested a protective role of SJMHE1 in excessive iodine-induced pyroptosis in TFCs, which might be attributed to its suppression for ROS/MAPK/NF-κB signaling pathway by binding of SJMHE1 with TLR2.
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