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ArticleNeurochemical research2025

Oxytocin Anti-Apoptotic Potential Mediates Neuroprotection Against 3-Nitropropionic Acid-Induced Huntington's Disease-Like Pathophysiology in Rats: Involvement of Calpain-2/p25 Cdk5/MEF-2 Signaling Pathway.

Marwa Rabie, Dalia M El-Tanbouly, Esraa A Kandil, Helmy M Sayed

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Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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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

4 authors.

Marwa RabiePharmacology and Toxicology Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini Street, 11562, Cairo, Egypt. marwa.rabie@std.pharma.cu.edu.eg.ORCID http://orcid.org/0009-0000-0253-4821
Dalia M El-TanboulyPharmacology and Toxicology Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini Street, 11562, Cairo, Egypt.
Esraa A KandilPharmacology and Toxicology Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini Street, 11562, Cairo, Egypt.
Helmy M SayedPharmacology and Toxicology Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini Street, 11562, Cairo, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increasing interest in the pro-apoptotic function of calpain-2 in the course of Huntington's disease (HD) is attributed to the involvement of its substrate, cyclin-dependent kinase 5 (Cdk5), in neuronal death during neurodegeneration. Oxytocin has been demonstrated to suppress apoptosis in many neurodegenerative disorders. This research aimed to investigate the effect of oxytocin on several calpain 2-induced apoptogenic factors in 3-nitropropionic acid (3-NP) animal model of HD in rats. For 14 days, rats received 3-NP (10 mg/kg, i.p.), and oxytocin (160 µg/kg, i.p.) 1 h before 3-NP administration. Oxytocin reversed the detrimental effects of 3-NP on the striatum, which was evidenced by improvement of motor behavior, as well as histological picture and neurochemical balance. Oxytocin markedly reduced striatal calpain-2 and p25 Cdk5 protein expressions and increased the endogenous calpain inhibitor, calpastatin expression along with the pro-survival factor, myocyte-enhancer factor 2 (MEF-2) contents. Moreover, it suppressed striatal content of the pro-apoptotic biomarkers (BCl-2-associated X protein (Bax), tumor suppressor protein (p53), and caspase-3) and elevated striatal anti-apoptotic B-cell lymphoma/leukemia 2 (BCl-2) content. It repressed the release of mitochondrial cytochrome c and apoptosis-inducing factor (AIF) to hinder caspase-dependent and caspase-independent apoptotic neuronal death. Oxytocin could be a promising candidate for HD management by hampering both mitochondrial and non-mitochondrial apoptosis through inhibition of calpain-2/p25 Cdk5/MEF-2 pathway.

Indexed as

ApoptosisCalpainHuntington DiseaseNeuroprotectionNeuroprotective AgentsOxytocinAnimalsCorpus StriatumCyclin-Dependent Kinase 5MaleNitro CompoundsPropionatesRatsRats, WistarSignal Transduction3-nitropropionic acidCalpainCapn2 protein, ratCdk5 protein, ratCyclin-Dependent Kinase 5Neuroprotective AgentsNitro CompoundsOxytocinPropionates3-NPApoptosisCalpain-2Huntington’s diseaseOxytocinp25 Cdk5

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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.