The effect of zinc acexamate on oxidative stress, inflammation and mitochondria induced apoptosis in rat model of renal warm ischemia - 11/07/18
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Graphical abstract |
Highlights |
• | Zinc acexamate preserves renal morphology and function after I/R. |
• | Zinc acexamate prevents I/R-induced oxidative stress. |
• | Zinc acexamate decreases the production of pro-inflammatory cytokines. |
• | Zinc acexamate improves mitochondrial membrane integrity and decreases apoptosis. |
Abstract |
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 induced-apoptosis. 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.
Le texte complet de cet article est disponible en PDF.Keywords : Zinc acexamate, Zinc, Ischemia reperfusion injury, Oxidative stress, Inflammation, Mitochondria
Plan
Vol 105
P. 573-581 - septembre 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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