Tyrosol attenuates ischemia-reperfusion-induced kidney injury via inhibition of inducible nitric oxide synthas.
Wang, P., Zhu, Q., Wu, N., Siow, Y.L., Aukema, H., and O, K. (2013). "Tyrosol attenuates ischemia-reperfusion-induced kidney injury via inhibition of inducible nitric oxide synthas.", Journal of Agricultural and Food Chemistry, 61(15), pp. 3669-3675. doi : 10.1021/jf400227u Access to full text
Tyrosol is a natural phenolic antioxidant compound. Oxidative stress represents one of the important mechanisms underlying ischemia–reperfusion-induced kidney injury. The aim of this study was to investigate the effect of tyrosol against ischemia–reperfusion-induced acute kidney injury. The left kidney of Sprague–Dawley rats was subjected to 45 min of ischemia followed by reperfusion for 6 h. Ischemia–reperfusion caused an increase in peroxynitrite formation and lipid peroxidation. The level of nitric oxide (NO) metabolites and the mRNA of inducible nitric oxide synthase (iNOS) were elevated in ischemia-reperfused kidneys. Administration of tyrosol (100 mg/kg body weight) to rats prior to the induction of ischemia significantly reduced peroxynitrite formation, lipid peroxidation, and the level of NO metabolites. Tyrosol administration also attenuated ischemia–reperfusion-induced NF-κB activation and iNOS expression. Such a treatment improved kidney function. Results suggest that tyrosol may have a protective effect against acute kidney injury through inhibition of iNOS-mediated oxidative stress.
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