Potential renoprotective effects of silymarin against vancomycin-induced nephrotoxicity in rats

Güzel, Sevda; Şahinoğulları, Zuhal Uçkun; Canacankatan, Necmiye; Antmen, Şerife Efsun; Kibar, Deniz; Yılmaz, Banu Coşkun

doi:10.1080/01480545.2019.1584208

Cited by 25 publications

(19 citation statements)

References 21 publications

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“…BUN and CREA values were elevated in rats treated with OTA. The CURC significantly reduced BUN and CREA values in the serum of rats treated with OTA and this, in accordance with several data in literature, could be due to a reduction in renal damage by the CURC [49][50][51]. The increase in CREA observed in rats treated with OTA is related to the GFR reduction, which is associated with oxygen free radical formation.…”

Section: Discussionsupporting

confidence: 90%

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

et al. 2020

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Ochratoxin A (OTA) is a powerful nephrotoxin and the severity of its damage to kidneys depends on both the dose and duration of exposure. According to the scientific data currently available, the mechanism of action still is not completely clarified, but it is supposed that oxidative stress is responsible for OTA-induced nephrotoxicity. Bioactive compound use has emerged as a potential approach to reduce chronic renal failure. Therefore, curcumin (CURC), due to its therapeutic effects, has been chosen for our study to reduce the toxic renal effects induced by OTA. CURC effects are examined in Sprague Dawley rats treated with CURC (100 mg/kg), alone or in combination with OTA (0.5 mg/kg), by gavage daily for 14 days. The end result of the experiment finds rats treated with OTA show alterations in biochemical and oxidative stress parameters in the kidney, related to a decrease in the Glomerular Filtration Rate (GFR). Conversely, the administration of CURC attenuates oxidative stress and prevents glomerular hyperfiltration versus the OTA group. Furthermore, kidney histological tests show a reduction in glomerular and tubular damage, inflammation and tubulointerstitial fibrosis. This study shows that CURC can mitigate OTA–induced oxidative damage in the kidneys of rats.

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Section: Discussionsupporting

confidence: 90%

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

et al. 2020

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“…In another report [24], the authors observed a hepatoprotective effect of silymarin protection by enhancing hepatic GSH levels. Moreover, treatment by silymarin showed marked nephroprotection via mitigation of MDA and NO levels in a model of drug-induced nephrotoxicity [56]. In addition, the hepatoprotective effects of silymarin were attributed to its cell membrane stabilizing and lipid-preserving effects in a CCl4induced liver toxicity model in rats [57].…”

Section: Discussionmentioning

confidence: 97%

Silymarin protects against sepsis-induced acute liver and kidney injury via anti-inflammatory and antioxidant mechanisms in the rat

Al-Kadi

Ahmed

El‐Tahawy

et al. 2020

Journal of advanced Biomedical and Pharmaceutical Sciences

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Sepsis is a leading cause of death among intensive care patients. During sepsis, exaggerated reaction to infection leads to massive production of reactive oxygen species and inflammatory mediators, which eventually leads to multiple organ damage. Silymarin is a well-known antioxidant and cytoprotective agent, which showed protective effects in different models of disease. Thus, we hypothesized that silymarin would be protective against sepsis-induced liver and kidney injury. Sepsis was induced in rats by the cecal ligation and puncture (CLP) method. Rats were divided into sham, CLP-non-treated and CLP treated with silymarin (100 mg/kg, i.p. 1 h following CLP). After 24 h, rats were euthanized for blood and tissue samples, which were used for assessment of MDA, NO, GSH, IL-6 and TNF-α levels and SOD activity, in addition to renal and hepatic function parameters. Survival study was conducted using another set of animals following the same previously mentioned procedure. Silymarin showed protective effects evidenced by enhanced overall survival following sepsis (80% in silymarin-treated vs. 20% in septic group), in addition to improvement of hepatic and renal function parameters and reduction of MDA, NO, IL-6 and TNF-α levels. Moreover, silymarin supported the endogenous antioxidant mechanisms via elevation of GSH levels and reinforcement of SOD activity. In conclusion, silymarin protects against sepsis-induced hepatic and renal injury, possibly via antioxidant and anti-inflammatory mechanisms.

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“…These studies have been reviewed in detail 111 . Since then, spirulina and pycnogenol , 112 mitoTEMPO, naringenin, 113 a free radical scavenger zingerone, 114, 115 DHA‐enriched phosphatidylcholine (DHA‐PC), 116 rutin, 117 and silymarin 118 have been evaluated in animal studies. In our opinion, the antioxidants that are most ready for clinical trials include preparations that are already clinically available, such as atorvastatin, vitamin C, vitamin E, N‐acetylcysteine, erythropoietin, and erdosteine.…”

Section: Potential Strategies For Preventionmentioning

confidence: 99%

Vancomycin‐Induced Kidney Injury: Animal Models of Toxicodynamics, Mechanisms of Injury, Human Translation, and Potential Strategies for Prevention

et al. 2020

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Vancomycin is a recommended therapy in multiple national guidelines. Despite the common use, there is a poor understanding of the mechanistic drivers and potential modifiers of vancomycin-mediated kidney injury. In this review, historic and contemporary rates of vancomycin-induced kidney injury (VIKI) are described, and toxicodynamic models and mechanisms of toxicity from preclinical studies are reviewed. Aside from known clinical covariates that worsen VIKI, preclinical models have demonstrated that various factors impact VIKI, including dose, route of administration, and thresholds for pharmacokinetic parameters. The degree of acute kidney injury (AKI) is greatest with the intravenous route and higher doses that produce larger maximal concentrations and areas under the concentration curve. Troughs (i.e., minimum concentrations) have less of an impact. Mechanistically, preclinical studies have identified that VIKI is a result of drug accumulation in proximal tubule cells, which triggers cellular oxidative stress and apoptosis. Yet, there are several gaps in the knowledge that may represent viable targets to make vancomycin therapy less toxic. Potential strategies include prolonging infusions and lowering maximal concentrations, administration of antioxidants, administering agents that decrease cellular accumulation, and reformulating vancomycin to alter the renal clearance mechanism. Based on preclinical models and mechanisms of toxicity, we propose potential strategies to lessen VIKI.

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Potential renoprotective effects of silymarin against vancomycin-induced nephrotoxicity in rats

Cited by 25 publications

References 21 publications

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

Silymarin protects against sepsis-induced acute liver and kidney injury via anti-inflammatory and antioxidant mechanisms in the rat

Vancomycin‐Induced Kidney Injury: Animal Models of Toxicodynamics, Mechanisms of Injury, Human Translation, and Potential Strategies for Prevention

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