Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Abstract

Abstract. The aim of this study was to investigate the effects of quercetin on nitric oxide synthase (NOS), nuclear factor-κB (NF-κB) and apoptosis in renal ischemia/reperfusion (I/R) injury in rats. A total of 42 Sprague-Dawley rats were divided into three groups. The control, I/R and I/R+quercetin (I/R+Q) groups were treated with quercetin (50 mg/kg intraperitoneal) 1 h prior to the induction of ischemia. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined by high-performance liquid chromatography (HPLC). p53, endothelial NOS (eNOS) and NF-κB expression were assessed immunohistochemically, and apoptosis assesment was performed using terminal deoxy nucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. The mRNA levels of inducible NOS (iNOS) in renal tissue were determined by realtime polymerase chain reaction (RT-PCR). MDA levels were significantly decreased in the quercetin group compared to the I/R group. However, GSH levels were significantly increased with quercetin treatment in the I/R group. Histological results, the number of apoptotic and p53-positive cells, NF-κB and eNOS expression levels were significantly decreased in the quercetin treatment group compared to the I/R group. iNOS gene expression increased in the I/R group, but no significant difference was found between the I/R and quercetin treatment groups. Therefore, quercetin not only has antioxidant and antiapoptotic activities, but also has an inhibitory effect on eNOS and NF-κB for renal tissue protection during I/R injury in rats. Therefore, quercetin may be a promising renoprotective therapeutic agent.

Effect of αlipoic acid and silymarin on bladder outlet obstruction

“…Data obtained previously has revealed that ischemic damage is involved with iNOS, while most iNOS is associated with inflammatory causes (22). However, the role of NO in BOO remains controversial.…”

Honokiol protects against renal ischemia/reperfusion injury via the suppression of oxidative stress, iNOS, inflammation and STAT3 in rats

“…In normal kidney tissues, endothelial NOS is predominantly expressed in the renal blood vessels and capillaries; neuronal NOS is predominantly expressed in the juxtaglomerular macula densa; and iNOS is expressed in the renal medullary thick ascending limb, proximal tubule, distal convoluted tubule and interlobular arteries, arcuate arteries and blood vessels, and other areas of the glomerulus (31). Under a pathophysiological state, iNOS exhibits high levels of expression in mesangial cells, epithelial cells, smooth muscle cells and renal tubular epithelial cells, and there are high levels of infiltrated inflammatory cells, including in the glomeruli and renal interstitium (32).…”

Protective Effect of Nicotinamide Adenine Dinucleotide Phosphate on Renal Ischemia-Reperfusion Injury

“…MDA results from lipid peroxidation and is generally employed as a biomarker of oxidative stress [29-31]. GSH is the main safeguard against oxidative damage by promoting the cellular system of protection against oxidative damage [32]. One related study showed that Vitamin C intake increased GSH levels after renal ischemia injury [33].…”