Brain injury · 2026
Intranasal administration of enalapril confers acute neuroprotection by mitigating mitochondrial dysfunction and apoptosis in a rat model of ischemic stroke.
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Sadeghian Nooshin, Salimpour Azar Saied, Shadman Javad, Abedi Ali, Salimi Ahmad, Alipour Mohammad Reza, Panahpour Hamdollah
Аннотация
BACKGROUND: Stroke remains a leading cause of mortality and long-term disability worldwide, with effective treatments hindered by its complex pathophysiology. This study is the first to explore the neuroprotective potential of intranasal enalapril, in mitigating ischemic stroke outcomes through its influence on mitochondrial function.
METHODS: Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO), followed by the intranasal administration of enalapril (0.03 mg/kg) post-ischemia. Neurological function was evaluated after 24 hours of reperfusion through the modified neurological severity score (mNSS), grip strength, and hot plate tests. Brain infarct volume was quantified via Triphenyltetrazolium chloride staining. Blood- brain barrier (BBB) integrity was evaluated via the Evans Blue extravasation assay. Additionally, we employed immunofluorescence techniques to assess apoptosis through TUNEL staining and evaluated mitochondrial function by examining mitochondrial swelling, succinate dehydrogenase activity, mitochondrial membrane potential and reactive oxygen species production.
RESULTS: Intranasal administration of enalapril significantly reduced the infarct volume, preserved BBB integrity, and attenuated sensorimotor deficits in MCAO rats. These protective effects were closely associated with enhanced regional cerebral blood flow, a significant reduction in neuronal apoptosis, and improved mitochondrial function.
CONCLUSION: Intranasal enalapril may provide a novel approach to neuroprotection in ischemic stroke, potentially through mechanisms that enhance mitochondrial function and reduce neuronal apoptosis.
METHODS: Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO), followed by the intranasal administration of enalapril (0.03 mg/kg) post-ischemia. Neurological function was evaluated after 24 hours of reperfusion through the modified neurological severity score (mNSS), grip strength, and hot plate tests. Brain infarct volume was quantified via Triphenyltetrazolium chloride staining. Blood- brain barrier (BBB) integrity was evaluated via the Evans Blue extravasation assay. Additionally, we employed immunofluorescence techniques to assess apoptosis through TUNEL staining and evaluated mitochondrial function by examining mitochondrial swelling, succinate dehydrogenase activity, mitochondrial membrane potential and reactive oxygen species production.
RESULTS: Intranasal administration of enalapril significantly reduced the infarct volume, preserved BBB integrity, and attenuated sensorimotor deficits in MCAO rats. These protective effects were closely associated with enhanced regional cerebral blood flow, a significant reduction in neuronal apoptosis, and improved mitochondrial function.
CONCLUSION: Intranasal enalapril may provide a novel approach to neuroprotection in ischemic stroke, potentially through mechanisms that enhance mitochondrial function and reduce neuronal apoptosis.