Evidence map›Paper›PMID 42758352›Full record

ArticleJournal of molecular histology2026

Histopathological and immunohistochemical characterization of MPTP-associated pancreatic injury and its attenuation by Hexarelin in mice.

Melda Şahin, Şenay Topsakal, Onur Elmas, Özlem Özmen

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Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

4 authors.

Melda ŞahinDepartment of Pathology, Faculty of Veterinary Medicine, University of Burdur Mehmet Akif Ersoy, Burdur, Turkey. meldasahin0510@gmail.com.
Şenay TopsakalDepartment of Endocrinology and Metabolism, Faculty of Medicine, Pamukkale University, Denizli, Turkey.
Onur ElmasDepartment of Physiology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
Özlem ÖzmenDepartment of Pathology, Faculty of Veterinary Medicine, University of Burdur Mehmet Akif Ersoy, Burdur, Turkey.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is associated with systemic inflammatory and metabolic alterations that may extend beyond the central nervous system. Although 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) reproduces several pathological features of Parkinsonian neurodegeneration, its effects on pancreatic tissue remain poorly characterized. This study investigated MPTP-associated pancreatic histopathological and immunohistochemical alterations and evaluated the potential attenuating effects of Hexarelin. Fifty male BALB/c mice were randomly assigned to five groups (n = 10/group): Sham, MPTP, Hexarelin, PreHexarelin, and PostHexarelin. Pancreatic tissues were examined using hematoxylin and eosin staining and immunohistochemistry for amylin, β-amyloid, caspase-3, glucagon, insulin, CD11b, CD68, interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α). MPTP administration was associated with marked pancreatic injury characterized by acinar degeneration, cytoplasmic vacuolization, vascular congestion, interstitial edema, inflammatory cell infiltration, and degeneration of the islets of Langerhans. Immunohistochemical analysis demonstrated increased inflammatory (CD11b, CD68, IL-1β, and TNF-α) and apoptosis-associated (caspase-3) marker immunoreactivity, together with increased β-amyloid immunoreactivity and decreased insulin and amylin immunoreactivities. Hexarelin treatment attenuated these histopathological and immunohistochemical alterations in both treatment groups, although the magnitude of improvement varied among individual markers. These findings suggest that MPTP exposure is associated with pancreatic inflammation, apoptosis-associated changes, and alterations in endocrine-marker immunoreactivity. Hexarelin treatment was associated with attenuation of these pathological changes and partial preservation of islet morphology and endocrine-marker immunoreactivity; however, the PostHexarelin findings should be interpreted cautiously because the absence of a sequence- and time-matched post-MPTP vehicle control prevents complete separation of Hexarelin-associated effects from temporal changes after MPTP administration.

Indexed as

PancreasAnimalsApoptosisCaspase 3ImmunohistochemistryInsulinInterleukin-1betaMaleMiceMice, Inbred BALB COligopeptidesCaspase 3hexarelinInsulinInterleukin-1betaOligopeptidesApoptosisHexarelinImmunohistochemistryMPTPPancreasPancreatic injury

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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.