Protective Effect of Quercetin on the Evolution of Cisplatin-Induced Acute Tubular Necrosis

Francescato, Heloı́sa Della Coletta; Coimbra, Terezila Machado; Costa, R. S.; Bianchi, María de Lourdes Pires

doi:10.1159/000078309

Cited by 63 publications

(44 citation statements)

References 56 publications

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“…The proximal tubular epithelial cells, in which CP is actively accumulated to levels 5-fold higher than that in serum [8], are known to be a major target for CP toxicity [9,10]. Although the nephrotoxic mechanisms of CP are not completely understood, several studies have reported involvement of the generation of free radicals including reactive oxygen species, disruption of mitochondrial function, depletion of anti-oxidant capacity, and activation of cell death machinery including apoptotic or necrotic pathways [11,12,13]. To develop novel strategies to prevent and/or reduce drug-induced AKI, diverse pharmacologic and molecular approaches have been investigated using CP-induced AKI [7]; however, the clinical applications of these preventive approaches are still limited [3].…”

Section: Introductionmentioning

confidence: 99%

Protective Activity of Dendropanax Morbifera Against Cisplatin-Induced Acute Kidney Injury

Kim

Lee²,

Akram

et al. 2015

Kidney Blood Press Res

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Background/Aims: Drug-induced acute kidney injury (AKI) has been a severe threat to hospitalized patients, raising the urgent needs to develop strategies to reduce AKI. We investigated the protective activity of Dendropanax morbifera (DP), a medicinal plant which has been widely used to treat infectious and pain diseases, on acute kidney injury (AKI) using cisplatin-induced nephropathic models. Methods: Both in vitro renal tubular cells (NRK-52E) and in vivo rat models were used to demonstrate the nephroprotective effect of DP. Results: Methanolic extract from DP significantly reduced cisplatin-induced toxicity in renal tubular cells. Through successive liquid extraction, the extract of DP was separated into n-hexane, CHCl₃, EtOAc, n-BuOH, and H₂O fractions. Among these, the CHCl₃ fraction (DPCF) was found to be most potent. The protective activity of DPCF was found to be mediated through anti-oxidant, mitochondrial protective, and anti-apoptotic activities. In in vivo rat models of AKI, treatment with DPCF significantly reversed the cisplatin-induced increase in blood urea nitrogen and serum creatinine and histopathologic damage, recovered the level of anti-oxidant enzymes, and inhibited renal apoptosis. Conclusion: We demonstrated that DP extracts decreased cisplatin-induced renal toxicity, indicating its potential to ameliorate drug-associated acute kidney damage.

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Section: Introductionmentioning

confidence: 99%

Protective Activity of Dendropanax Morbifera Against Cisplatin-Induced Acute Kidney Injury

Kim

Lee²,

Akram

et al. 2015

Kidney Blood Press Res

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“…Various other studies have also demonstrated the beneficial effect of quercetin in reducing cisplatin-induced acute tubular necrosis and nephrotoxicity without compromising its antitumor effects. 10,11 To date, the in vivo effect of quercetin on fluoride nephrotoxicity and redox parameters has not yet been established, and this study was primarily designed to address this key pharmacological parameters. It is also well known that vitamin C has a nephroprotective role in NaF-induced nephrotoxicity and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Ameliorative Effects of Quercetin on Sodium Fluoride-Induced Oxidative Stress in Rat’s Kidney

et al. 2012

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Objective: The in vivo nephroprotective effect of quercetin against sodium fluoride (NaF)-induced damage was studied. Methods: Renal injury was induced by daily administration of NaF (600 ppm) through drinking water for 1 week. The levels of reduced glutathione (GSH), lipid peroxidation as well as superoxide dismutase and catalase activity of kidney homogenates were determined. The serum markers of glomerular damage, including creatinine, serum urea, and blood urea nitrogen levels, were also assessed. Results: The study revealed that administration of fluoride resulted in a significant downregulation of antioxidant defenses coupled with an increased serum level of glomerular damage markers. The administration of quercetin prior to fluoride reversed the antioxidant-oxidant balance to control (fluoride-untreated) level. The level of protection obtained for the 20 mg/kg quercetin treatment was equivalent to the positive control, ascorbic acid (10 mg/kg). The therapeutic implication of antioxidants in fluoride-induced nephrotoxicity is discussed. Conclusions: This study showed that NaF intoxication caused renal damage by increasing oxidative stress, and quercetin and vitamin C administration gave protection against fluoride-induced oxidative stress to some degree.

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“…The first group served as control, which received the vehicle only (0.9% NaCl, 0.25 ml intraperitoneally for 5 days), Groups 2 and 3 were administered orally quercetin at a dose of 50 mg/kg bwt (Francescato et al, 2004) or lecithin at a dose of 100 mg/kg bwt (Lee et al, 2013 ) suspended in distilled water, respectively for six days whereas group 4 was used as positive control were administered ifosfamide at a dose of 80mg/kg bwt (Chen et al, 2008 ) intraperitoneally for five days. Groups 5 and 6 were administered either quercetin or lecithin along with ifosfamide by the same treatments regimens, respectively.…”

Section: Drug Treatmentsmentioning

confidence: 99%

Evaluation of the protective role of quercetin and lecithin on Ifosfamide neurotoxicity in rats

Nashwah¹,

Lobna²,

Sabry³

2016

Int. J. Adv. Res. Biol. Sci.

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Objective: The present study aimed to contribute the ability of quercetin and /or lecithin to attenuate ifosfamide neurotoxicity. Seventy female albino rats were randomly divided into seven groups. Ifosfamide (IFO; 80mg/kg b.wt.) was administrated for five consecutive days intraperitoneally (i.p.), while quercetin (50mg/kg b.wt.) and lecithin (100mg/kg b.wt) were given orally either singly or in-combination with IFO for six consecutive days. Results: Ifosfamide induce neural toxicity as indicated by decreased GSH/GSSG ratio and elevated NO level in different brain areas. As well as altering neurotransmitters levels accompanied by inhibition of choline esterase activity in serum. Also, it stimulates an apoptotic signaling program by up-regulation of caspase-3 and assimilation of Bcl-2 gene expression in all tested brain areas. Pretreatment with quercetin and lecithin singly or incombination could attenuate ifosfamide neurotoxicity by variable degrees of improvement. This improvement seems to be a parameter selective among different brain areas. Conclusion: The present study concludes that pretreatment with combined therapy showed more pronounced effect compared to singular one. Therefore, we suggested that the synergistic effect of quercetin and lecithin in the combined treatment results in marked neuroprotective effect in part through their antioxidant properties and intervening in apoptotic pathways.

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Protective Effect of Quercetin on the Evolution of Cisplatin-Induced Acute Tubular Necrosis

Cited by 63 publications

References 56 publications

Protective Activity of <b><i>Dendropanax Morbifera</i></b> Against Cisplatin-Induced Acute Kidney Injury

Protective Activity of <b><i>Dendropanax Morbifera</i></b> Against Cisplatin-Induced Acute Kidney Injury

Ameliorative Effects of Quercetin on Sodium Fluoride-Induced Oxidative Stress in Rat’s Kidney

Evaluation of the protective role of quercetin and lecithin on Ifosfamide neurotoxicity in rats

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