Purpose: To investigate the protective effect of dexmedetomidine (Dex) on testicular damage induced by ischemia-reperfusion injury in rats.
Methods: Sham group underwent left scrotal exploration only (group 1). The ischemia-reperfusion only group underwent left testicular torsion and detorsion (group 2). The ischemia-reperfusion plus Dex group underwent left testicular torsion, received 50 µg/kg Dex (group 3) and 100 µg/kg Dex (group 4) intraperitoneally at minute 180 of ischemia and then underwent detorsion. We determined histopathological findings and performed specific biochemical analyses.
Results: Increasing doses of Dex significantly increased TAS, and significantly decreased OSI. Analyzing the antioxidant effects of increasing doses of Dex in torsion and contrlateral testicles: Dex 100 µg/kg statistically significant increased the tissue total antioxidant status (TAS) and oxidative stress index (OSI) when compared with Dex 50 µg/kg but not found significantly change on the tissue total oxidant status (TOS). However, Dex did not significantly improve these histological alterations.
Conclusion: The antioxidant effects of dexmedetomidine on testicular ischemia-reperfusion injury in ipsilateral and contrlateral testis, but in the histopathological level, there was no difference statistically according to Johnsen's scoring system between groups at both sides.
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http://dx.doi.org/10.1590/S0102-865020150060000007 | DOI Listing |
Redox Rep
December 2025
Department of Cardiology, Fujian Medical University Union Hospital, Fuzhou, Fujian, People's Republic of China.
Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.
Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model.
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Physiology, College of Medicine, King Saud University, 12271, Riyadh, Saudi Arabia.
Ischemia-reperfusion injury (IRI) is a common pathogenic situation that arises throughout all liver surgeries, including liver transplants. We aimed to compare the preventive effects of valsartan (VST) against valsartan + sacubitril (LCZ696) on hepatic injury caused by IRI. A total of thirty-six male Westar albino rats were split into six groups randomly: sham, IRI, VST + IRI, LCZ696 + IRI, VST, and LCZ696.
View Article and Find Full Text PDFNeurosci Bull
January 2025
Liaoning Provincial Key Laboratory of Cerebral Diseases, Department of Physiology, College of Basic Medical Sciences, Dalian Medical University, Dalian, 116044, China.
Drug Des Devel Ther
January 2025
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
Purpose: This study aimed to assess the protective effect of a clinical dose esketamine on cerebral ischemia/reperfusion (I/R) injury and to reveal the potential mechanisms associated with microglial polarization and autophagy.
Methods: Experimental cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in adult rats and simulated by oxygen-glucose deprivation (OGD) in BV-2 microglial cells. Neurological and sensorimotor function, cerebral infarct volume, histopathological changes, mitochondrial morphological changes, and apoptosis of ischemic brain tissues were assessed in the presence or absence of esketamine and the autophagy inducer rapamycin.
World J Stem Cells
January 2025
Internal Medicine-II, Paracelsus Medical University Salzburg, Salzburg 5020, Austria.
Increasing evidence of the significant clinical value of protection against ischemia/reperfusion injury has contributed to the realization of the independent importance of this approach in improving prognosis and reducing cardiovascular mortality. Extracellular vesicles (EVs) derived by adipose mesenchymal stem cells may mediate the paracrine effects of stem cells and provide regenerative and anti-inflammatory properties, which are enhanced by γ-aminobutyric acid. The protective effects on cardiac myocytes may result from the EV embarked by miR-21-5p, which is a target for thioredoxin-interacting protein, regulating the formation of thioredoxin-interacting protein-thioredoxin complexes and subsequently enhancing the antioxidant activity of thioredoxin.
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