Inhibiting Soluble Epoxide Hydrolase Suppresses NF-κB p65 Signaling and Reduces CXCL10 Expression as a Potential Therapeutic Target in Hashimoto's Thyroiditis
Authors' conclusion
Our findings suggest that sEH/NF-κB p65/CXCL10-CXCR3 might be promising therapeutic targets for HT.
Study context
- Population
- Patients with Hashimoto's thyroiditis and healthy controls; thyroid follicular epithelial cells (TFECs) and rat Hashimoto's thyroiditis (HT) model
- Comparison
- HT vs healthy controls; Adamantyl-ureido-dodecanoic acid (AUDA) soluble epoxide hydrolase (sEH) inhibition in TFECs and rat HT model
Methodological detailshuman tissue, TFEC and rat HT model experiments
- Human tissue, TFEC and rat HT model experiments
Main finding
As reported in the abstract
- sEH significantly upregulated in HT patients vs healthy individuals
- Transcriptome sequencing: cytokine-related pathways and chemokine expression aberrant in HT, especially CXCL10 and its receptor CXCR3
- In TFECs and rat HT model, blocking sEH with AUDA inhibited autoantibody, NF-κB signaling, CXCL10/CXCR3 expression and type-1 helper CD4+ T cells
Original publication
Inhibiting Soluble Epoxide Hydrolase Suppresses NF-κB p65 Signaling and Reduces CXCL10 Expression as a Potential Therapeutic Target in Hashimoto's Thyroiditis. J Clin Endocrinol Metab. Published 13 March 2024. doi:10.
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