The protective effect of erdosteine against cyclosporine A-induced cardiotoxicity in rats

Selçoki, Yusuf; Uz, Ebru; Bayrak, Reyhan; Sahin, Şevki; Kaya, Arif; Uz, Burak; Karanfil, Aydın; Özkara, Adem; Akçay, Ali

doi:10.1016/j.tox.2007.06.096

Cited by 33 publications

(33 citation statements)

References 30 publications

(23 reference statements)

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“…These observations are in agreement with the previous studies that demonstrated significant changes in hepatic [15], renal [2,35] and cardiac [29,36] functional parameters in the experimental animals after cyclosporine A administration.…”

Section: Discussionsupporting

confidence: 93%

Amelioration of Cyclosporine A‐Induced Renal, Hepatic and Cardiac Damages by Ellagic Acid in Rats*

Yüce¹,

Ateşşahín

Çeribaşı

2008

Basic Clin Pharma Tox

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Treatment with cyclosporine A has significantly improved long-term survival after organ transplantations. Cyclosporine A also causes a dose-related decrease in body functions in experimental animals and human beings. The generation of reactive oxygen species has been implicated in cyclosporine A-induced dysfunctions. The aim of this study was to determine the effects of ellagic acid on cyclosporine A-induced alterations in the kidney, liver and heart oxidant/antioxidant system. The control group was treated with placebo and subcutaneous injection of 0.5 ml isotonic saline + 0.5 ml slightly alkaline solution for 21 days. The cyclosporine A group received a subcutaneous injection of cyclosporine A (15 mg/kg) + 0.5 ml slightly alkaline solution for 21 days. The ellagic acid group was treated with a subcutaneous injection of 0.5 ml isotonic saline + ellagic acid (10 mg/kg) for 21 days. The cyclosporine A plus ellagic acid group received a subcutaneous injection of cyclosporine A + ellagic acid for 21 days. Ellagic acid and slightly alkaline solution were administered by gavage. The rats were killed at the end of the treatment period. Malondialdehyde (MDA) and reduced glutathione (GSH) levels, glutathione peroxidase (GSH-Px) and catalase (CAT) activities were determined in kidney, liver and heart tissues. While administration of cyclosporine A increased the MDA levels in kidney, liver and heart tissues, it decreased the GSH, GSH-Px and CAT in these samples when compared to the control group. However, the simultaneously administration of ellagic acid markedly normalized the cyclosporine A-induced liver and heart MDA levels, liver CAT activities and GSH-Px activities of all samples. Cyclosporine A caused marked damages in the histopathological status of kidney, liver and heart tissues, which were partially ameliorated by ellagic acid administration. In conclusion, ellagic acid may be used in combination with cyclosporine A in transplantation treatment to improve the cyclosporine A-induced oxidative stress parameters and other adverse effects.

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Section: Discussionsupporting

confidence: 93%

Amelioration of Cyclosporine A‐Induced Renal, Hepatic and Cardiac Damages by Ellagic Acid in Rats*

Yüce¹,

Ateşşahín

Çeribaşı

2008

Basic Clin Pharma Tox

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“…In this study, we demonstrated that MDA levels in the CsA group were significantly higher than in the control group. Previous studies have reported that increased MDA levels in CsA-treated rats may also correlate with oxidative damage in many tissues [2,6,7,27]. Importantly, we found that UDCA, melatonin, and allopurinol significantly reduced MDA production in liver.…”

Section: Discussionsupporting

confidence: 61%

Effects of antioxidant agents against cyclosporine-induced hepatotoxicity

Akbulut

Elbe

Eris

et al. 2015

Journal of Surgical Research

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“…5 of erdosteine metabolites for various drug-induced conditions including cardiotoxicity, hepatotoxicity, nephrotoxicity, and ischemia-reperfusion injury (Erarslan et al 2011;Fadillioglu et al 2003;Lee et al 2010;Ozyurt et al 2004;Selcoki et al 2007). Furthermore, oral treatment with erdosteine, attenuated the increase in serum creatinine level following an intraperitoneal injection of cisplatin , and prevented cisplatin-induced in vivo nephrotoxicity and hepatic oxidative injury in rats (Koc et al 2005;Ozyurt et al 2004).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Erdosteine protects HEI-OC1 auditory cells from cisplatin toxicity through suppression of inflammatory cytokines and induction of Nrf2 target proteins

Kim

Park

Lee

et al. 2015

Toxicology and Applied Pharmacology

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The protective effect of erdosteine against cyclosporine A-induced cardiotoxicity in rats

Cited by 33 publications

References 30 publications

Amelioration of Cyclosporine A‐Induced Renal, Hepatic and Cardiac Damages by Ellagic Acid in Rats*

Amelioration of Cyclosporine A‐Induced Renal, Hepatic and Cardiac Damages by Ellagic Acid in Rats*

Effects of antioxidant agents against cyclosporine-induced hepatotoxicity

Erdosteine protects HEI-OC1 auditory cells from cisplatin toxicity through suppression of inflammatory cytokines and induction of Nrf2 target proteins

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