ArticleNaunyn-Schmiedeberg's archives of pharmacology2021
Can MitoTEMPO protect rat sciatic nerve against ischemia-reperfusion injury?
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Conduction Velocity Distribution Reveals Fast-Fiber-Dominant Dysfunction in Acrylamide-Induced Peripheral Neurotoxicity.Brain sciences · 2026Article
- ACLY alleviates cerebral ischemia/reperfusion injury by reducing oxidative stress and enhancing mitochondrial function via histone acetylation.Cell death & disease · 2026Article
- Therapeutic comparison of MitoTEMPO and rosmarinic acid as mitochondria targeted and non targeted antioxidants evaluated in rat sciatic nerve crush injury model.Scientific reports · 2025Article
- Enhancing diabetic rat peripheral nerve conduction velocity parameters through the potent effects of MitoTEMPO.Heliyon · 2024Article
- Protective vs. Therapeutic Effects of Mitochondria-Targeted Antioxidant MitoTEMPO on Rat Sciatic Nerve Crush Injury: A Comprehensive Electrophysiological Analysis.Biomedicines · 2023Article
- Common methods in mitochondrial research (Review).International journal of molecular medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abdominal ischemia-reperfusion (I/R) is known to cause both structural and functional damage to sciatic nerve which is related to the oxidative stress. We investigated the protective effects of mitochondria-targeted antioxidant (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride (MitoTEMPO) on ischemia-reperfusion-induced nerve damage by using the conduction velocity distribution (CVD) calculations from in vitro compound nerve action potential (CNAP) recordings from rat sciatic nerve. Adult male Wistar albino rats were divided into three groups. The IR and IR + MT groups had aortic cross-clamping for 1 h followed by 2 h reperfusion, while SHAM group had the same procedure without cross-clamping. IR + MT group received 0.7 mg/kg/day MitoTEMPO injection for 28 days before I/R, while other groups received vehicle alone. Ischemia-reperfusion resulted in a significant decrease (p < .05) in maximum depolarizations (mV), areas (mV.ms), and maximum and minimum upstroke velocities (mV/ms) of CNAPs, while injection of MitoTEMPO showed a complete protective effect on these impairments. The histograms for CVD showed that I/R blocked the contribution of fast-conducting fibers (> 60 m/s). MitoTEMPO prevented that blockage and caused a shift in the CVD. Functional nerve damage caused by I/R can be prevented by MitoTEMPO, which can enter mitochondria, the main source of reactive oxygen species (ROS).
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Registered trials
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