The effect of zinc acexamate on oxidative stress, inflammation and mitochondria induced apoptosis in rat model of renal warm ischemia
Autor: | Carmen García Ruiz, Imed Messaoudi, Anna Baulies, Mohamed Amine Zaouali, Safa Ben Mimouna, Hassen Ben Abdennebi, José C. Fernández-Checa, Mohamed Bejaoui, Najet Hadj Abdallah, Ahlem Bouhlel |
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Přispěvatelé: | Ministère de l’Enseignement Supérieur et de la Recherche Scientifique (Tunisie), Ministerio de Economía y Competitividad (España), Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (España), National Institute on Alcohol Abuse and Alcoholism (US), National Institutes of Health (US), Generalitat de Catalunya |
Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
Male
0301 basic medicine medicine.medical_specialty Antioxidant medicine.medical_treatment Ischemia Apoptosis Inflammation Mitochondrion Kidney medicine.disease_cause Antioxidants 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine medicine Animals Warm Ischemia Rats Wistar Aminocaproates Pharmacology chemistry.chemical_classification Dose-Response Relationship Drug General Medicine Glutathione medicine.disease Mitochondria Disease Models Animal Zinc 030104 developmental biology Enzyme Endocrinology chemistry Oxidative stress Reperfusion Injury 030220 oncology & carcinogenesis Cytokines Zinc acexamate medicine.symptom Ischemia reperfusion injury |
Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname |
Popis: | Aim: Zinc has proved its efficacy in many models of ischemia reperfusion (I/R) injury. In this study, we used zinc acexamate (ZAC) as an exogenous source of zinc against renal I/R injury and we investigated whether its protective effects are mediated by the decrease of oxidative stress, inflammation, and mitochondria inducedapoptosis. Methods: Rats were orally pretreated with vehicle or ZAC (10 or 100 mg/kg) 24 h and 30 min prior to 1 h of bilateral renal warm ischemia and 2 h of reperfusion. Results: Our data showed that 10 mg/kg of ZAC, but not 100 mg/kg, improved renal architecture and function. Also, the low dose of ZAC up-regulated antioxidant enzymes activities and glutathione level and decreased lipids and proteins oxidation. Interestingly, the use of ZAC resulted in a significant reduce of pro-inflammatory cytokines (IL-1ß, IL-6 and MCP-1), enhanced mitochondria integrity and decreased expression of the pro-apoptotic protein caspase-9. Conclusion: We conclude that renal I/R induced oxidative stress, inflammation and apoptosis and that the use of ZAC at 10 mg/kg, but not 100 mg/kg, protects rat kidneys from I/R injury by down-regulating these processes. This work was supported by grants from: The Tunisian Ministry of Higher Education and Scientific Research (UR12ES11); SAF-2014- 57674-R, SAF-2015-69944-R from Plan Nacional de I + D, Spain and CIBEREHD; the center grant P50AA011999 Southern California Research Center for ALPD and Cirrhosis funded by NIAAA/NIH; and AGAUR of the Generalitat de Catalunya2014-SGR785. |
Databáze: | OpenAIRE |
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