ArticleScientific reports2026
Potential gonadal-beneficial effect of sitagliptin against paclitaxel-induced testicular dysfunction via mediating PERK/CHOP/NLRP3/Sestrin2 signaling pathway.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Combination of sitagliptin and mangiferin mitigates testicular damage induced by paclitaxel via mediating Sestrin2/Keap1/Nrf2 signaling pathway.Molecular and cellular biochemistry · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paclitaxel (PTX) is broadly prescribed to treat various malignancies. However, it induces negative impacts on many organs, including testes. This study explored the beneficial role of sitagliptin (SIT) in PTX-provoked testicular damage and the underlying mechanisms. Rats were allocated into four groups: (I) control, (II) PTX, (III) PTX + SIT5, and (IV) PTX + SIT10. Histopathological and ultrastructural analyses were conducted along with sperm analysis. Immunohistochemical examinations of NOD-like receptor protein 3 (NLRP3), cleaved caspase-3, caspase-3, cytochrome c (Cyt.c), and interleukin-1 beta (IL-1β) were assessed. Serum testosterone and testicular 17β-hydroxy steroid dehydrogenase (17β-HSD), sestrin2, phosphorylated protein kinase R-like ER kinase (pPERK), and C/EBP homologous protein (CHOP) were determined. SIT induced a remarkable increase in sperm count, motility, and viability, with a pronounced decline in sperm abnormality compared to PTX group. SIT increased testosterone and 17β HSD levels. SIT elevates sestrin2, reduced glutathione (GSH), and catalase, and reduces malondialdehyde (MDA), reflecting its antioxidant action. SIT mitigates ER stress via diminishing pPERK and CHOP. SIT reduces NLRP3 and IL-1β levels, clarifying its anti-inflammatory action. SIT decreases cleaved caspase-3, caspase-3, and Cyt.c levels, verifying its anti-apoptotic features. Overall, SIT ameliorated PTX-provoked testicular dysfunction via mediating PERK/CHOP/NLRP3/Sestrin2 signaling pathway.
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