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.
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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Who cites it
2 citing papers in PubMed.
- Oxytocin restores cognitive function and attenuates neuroinflammation in chronic sleep-deprived aged rats.Frontiers in aging neuroscience · 2026Article
- Salidroside derivative SHPL-49 enhances synaptic remodeling in BCCAO rats via the CDK5/p35/p25 signaling pathway.Frontiers in pharmacology · 2026Article
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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.
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