Protective effects of thymoquinone on vancomycin-induced nephrotoxicity in rats

Başarslan, Fatmagül; Yılmaz, Nigar; Ateş, Şükrü; Özgür, Tümay; Tutanç, Murat; Motor, Vicdan Köksaldı; Arıca, Vefik; Yılmaz, Cahide; İnci, Melek; Büyükbaş, Sadık

doi:10.1177/0960327111433185

Cited by 65 publications

(54 citation statements)

References 38 publications

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“…It has been reported also in the previous studies that a reduction also occurred in levels of compounds with antioxidant characteristics such as selenium 37 and glutathione 38,39 as well as decreased antioxidant enzyme activities in the rat tissues exposed to arsenic. [39][40][41] Contrarily, it has been encountered in the arsenic + TQ group that tissue MDA level decreased, while a significant elevation was encountered in the antioxidant enzyme activities (SOD and CAT) when compared with the arsenic group. There are some studies in the literature that supported the results of antioxidant enzyme activities encountered in this study.…”

Section: Discussionmentioning

confidence: 99%

“…Elsherbiny and El-Sherbiny 35 have reported in their study that they observed increased activities of the antioxidant enzymes such as SOD and glutathione-S-transferase beside a reduction in the activity of the oxidant enzyme NADPH oxidase in the group treated with TQ against oxidative kidney injury caused by doxorubicin. Basarslan et al 40 have reported that negative changes observed in the activities of SOD and GSH-PX in the renal tissue caused by vancomycin was prevented by TQ. Prabhakar et al 41 have shown in their study that decreased activities of SOD and CAT in the liver tissue caused by highdose fructose diet was prevented with the treatment of TQ.…”

Section: Discussionmentioning

confidence: 99%

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Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

et al. 2015

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We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

et al. 2015

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“…Numerous therapeutic agents have been investigated clinically and experimentally against this adverse effect, however, none of them confirmed to be clinically effective as a 4 Jundishapur J Nat Pharm Prod. In Press(In Press):e67178.…”

Section: Discussionmentioning

confidence: 99%

“…This dose of VCM was selected based on previous studies (4,6,8,9). The rats were weighed prior to the first injection of VCM and every other day in order to adjust the dose according to weight changes.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…One of the major adverse effects of this drug is nephrotoxicity, which has limited its dose and duration of administration (1,2). Although the exact mechanism of renal toxicity of VCM is not fully understood, some published studies have suggested that the oxidative stress has a crucial role in the pathogenesis of VCM-induced nephrotoxicity (VIN) (3)(4)(5)(6)(7). Several antioxidants including: vitamin E (8), 2, 3-dihydroxybenzoic acid (9), curcumin (10) and vitamin C (11) have been reported that reduces VIN.…”

Section: Introductionmentioning

confidence: 99%

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Nephroprotective Effect of Nasturtium Officinale (Watercress) Ethanol Extract and Vitamin E on Vancomycin-Induced Nephrotoxicity in Rats

Karami

Mostafazadeh

Sadeghi

et al. 2018

Jundishapur J Nat Pharm Prod

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Background: Vancomycin (VCM) is an important antibiotic that is active against gram-positive cocci, and its nephrotoxicity remain as a major problem in clinical use. Objectives: This study was designed to investigate the effect of Nasturtium officinale hydro-alcoholic extract (NOE) and vitamin E aganist VCM-induced nephrotoxicity in adult male wistar rats. Methods: A total of 36 animals were randomly divided into 6 equal groups (n = 6) including 1, control group; 2, VCM group; 3, VCM + NOE (250 mg/kg) group; 4, VCM + NOE (500 mg/kg) group; 5, VCM + vitamin E (250 mg/kg) group; and 6, VCM + vitamin E (500 mg/kg) group. VCM (200 mg kg -1 i.p.) was given every 12 hours for 7 consecutive days. NOE and vitamin E were orally given to rats 30

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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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Protective effects of thymoquinone on vancomycin-induced nephrotoxicity in rats

Abstract: These results indicate that the TQ produces a protective mechanism against VCM-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

Cited by 65 publications

References 38 publications

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

Nephroprotective Effect of Nasturtium Officinale (Watercress) Ethanol Extract and Vitamin E on Vancomycin-Induced Nephrotoxicity in Rats

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

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