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  3. Protective effect of MitoTEMPO against cardiac dysfunction caused by ischemia-reperfusion: MCAO stroke model study

Protective effect of MitoTEMPO against cardiac dysfunction caused by ischemia-reperfusion: MCAO stroke model study

  • Int J Neurosci. 2024 Dec;134(12):1582-1593. doi: 10.1080/00207454.2023.2273768.
Ahmet Akkoca 1,  Belgin Büyükakıllı 2,  Ebru Ballı 3,  Burcu Gültekin 4,  Erkan Özbay 5,  Hatice Oruç Demirbağ 3,  Çağatay Han Türkseven 2
Affiliations

Affiliations

  • 1 Department of Occupational Health and Safety, Taşkent Vocational School, Selcuk University, Konya, Türkiye.
  • 2 Department of Biophysics, Faculty of Medicine, Mersin University, Mersin, Türkiye.
  • 3 Department of Histology and Embryology, Faculty of Medicine, Mersin University, Mersin, Türkiye.
  • 4 Department of Histology and Embryology, Faculty of Medicine, Necmettin Erbakan University, Konya, Türkiye.
  • 5 Department of Medical Services and Techniques, Health Services Vocational School, Karamanoğlu Mehmetbey University, Karaman, Türkiye.
PMID: 37862003 DOI: 10.1080/00207454.2023.2273768
Abstract

Purpose: Neurological impairments are the leading cause of post-stroke mortality, while stroke-related cardiovascular diseases rank second in significance. This study investigates the potential protective effects of MitoTEMPO (2,2,6,6-tetramethyl-4-[[2-(triphenylphosphonio) acetyl] amino]-1-piperidinyloxy, monochloride, monohydrate), a mitochondria-specific antioxidant, against cardiac and neurological complications following stroke. The objective is to assess whether MitoTEMPO can be utilized as a protective agent for individuals with a high risk of stroke.

Materials and methods: Seventeen-week-old male Wistar Albino rats were randomly assigned to three groups: SHAM, ischemia-reperfusion and MitoTEMPO + ischemia-reperfusion (MitoTEMPO injection 0.7 mg/kg/day for 14 days). The SHAM group underwent a sham operation, while the ischemia-reperfusion group underwent 1-h middle cerebral artery occlusion followed by three days of reperfusion. Afterwards, noninvasive thoracic electrical bioimpedance and electrocardiography measurements were taken, and sample collection was performed for histological and biochemical examinations.

Results: Our thoracic electrical bioimpedance and electrocardiography findings demonstrated that MitoTEMPO exhibited a protective effect on most parameters affected by ischemia-reperfusion compared to the SHAM group. Furthermore, our biochemical and histological data revealed a significant protective effect of MitoTEMPO against oxidative damage.

Conclusions: The findings suggest that both ischemia-reperfusion-induced cardiovascular abnormalities and the protective effect of MitoTEMPO may involve G-protein coupled receptor-mediated signaling mechanisms. This study was conducted with limitations including a single gender, a uniform age group, a specific stroke model limited to middle cerebral artery, and pre-scheduled only one ischemia-reperfusion period. In future studies, addressing these limitations may enable the implementation of preventive measures for individuals at high risk of stroke.

Keywords

Cardiovascular disease; ischemic stroke; middle cerebral artery occlusion.

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