Neuroprotective Effects of Bromelain on Acute Ischemic Stroke in Rats

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dc.contributor.authorKorkmaz, Engin
dc.contributor.authorBeytur, Asiye
dc.contributor.authorTekin, Suat
dc.date.accessioned2026-04-04T13:35:16Z
dc.date.available2026-04-04T13:35:16Z
dc.date.issued2026
dc.departmentİnönü Üniversitesi
dc.description.abstractIschemic stroke (IS) is a severe neurological disorder that develops as a result of the interruption of cerebral blood flow and leads to high rates of mortality and morbidity. This study examined the neuroprotective potential of bromelain (Brm) in a rat model of IS induced by middle cerebral artery occlusion (MCAO). Three-month-old male Sprague Dawley rats were divided into four groups: Sham, IS, Brm20 + IS, and Brm40 + IS (n = 10 per group). Brm (20 or 40 mg/kg) or vehicle was administered orally for seven days prior to surgery, followed by 60 min of transient MCAO and 24 h of reperfusion. During reperfusion, neurological deficit scores and rotarod performance were assessed, and infarct volume was determined using 2,3,5-triphenyltetrazolium chloride staining. In the IS group, neurological deficits and infarct volume were significantly increased. The oxidative stress marker malondialdehyde (MDA) and pro-inflammatory cytokines (TNF-alpha, IL-1 beta, IL-6) were elevated, whereas the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), as well as the anti-apoptotic protein Bcl-2, were reduced. In addition, apoptotic markers (Bax, caspase-3) and angiogenic markers, including vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9), were increased, while the activity of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling was suppressed. Brm treatment attenuated these pathological alterations by reducing angiogenesis, inflammation, and apoptosis, enhancing antioxidant defense, and restoring PI3K/Akt signaling activity. In conclusion, the present study demonstrated that Brm exerts multifaceted neuroprotective effects in experimental IS by targeting key mechanisms including oxidative stress, inflammation, apoptosis, angiogenesis, and PI3K/Akt signaling. These findings suggest that Brm may represent a potential pharmacological candidate for the treatment of IS, pending validation in future advanced preclinical and clinical studies.
dc.description.sponsorshipInonu University Scientific Research Projects Unit [TDP-2024-3628]
dc.description.sponsorshipThis study was supported by Inonu University Scientific Research Projects Unit (Project No: TDP-2024-3628).
dc.identifier.doi10.1007/s44411-025-00468-z
dc.identifier.endpage662
dc.identifier.issn0006-9248
dc.identifier.issn1336-0345
dc.identifier.issue2
dc.identifier.orcid0000-0002-8365-2914
dc.identifier.scopus2-s2.0-105024887265
dc.identifier.scopusqualityQ2
dc.identifier.startpage651
dc.identifier.urihttps://doi.org/10.1007/s44411-025-00468-z
dc.identifier.urihttps://hdl.handle.net/11616/109724
dc.identifier.volume127
dc.identifier.wosWOS:001638813700001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherSpringernature
dc.relation.ispartofBratislava Medical Journal
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250329
dc.subjectBromelain
dc.subjectInflammation
dc.subjectIschemic Stroke
dc.subjectNeuroprotection
dc.subjectOxidative stress
dc.titleNeuroprotective Effects of Bromelain on Acute Ischemic Stroke in Rats
dc.typeArticle

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