Caffeic Acid Phenethyl Ester Protects Kidneys against Acetylsalicylic Acid Toxicity in Rats

Bozkurt, Yaşar; Bozkurt, Mehtap; Türkçü, Gül; Sancaktutar, Ahmet Ali; Söylemez, Haluk; Penbegül, Necmettin; Atar, Murat; Bodakçı, Mehmet Nuri; Hatipoğlu, Namık Kemal; Yüksel, Hatice; Kibrisli, Erkan; Yavuz, Celal

doi:10.3109/0886022x.2012.717485

Cited by 7 publications

(5 citation statements)

References 22 publications

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“…There have also been different clinical studies on TAS and TOS measurements as an indicator of oxidative/antioxidative balance ( 38 - 40 ). In experimental studies investigating the relationship between oxidative stress following toxic exposure and nephrotoxicity, we observe that while the TOS level increased significantly in the presence of oxidative stress, the TAS level decreased significantly ( 41 , 42 ). However, we could not find any studies in the literature investigating TAS and TOS activity in renal cells following in vivo α-AMA exposure.…”

Section: Discussionmentioning

confidence: 91%

Alpha-Amanitin Poisoning, Nephrotoxicity and Oxidative Stress: An Experimental Mouse Model

Ergin

Dündar

Kılınç

et al. 2015

Iran Red Crescent Med J

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Background:Alpha-amanitin (α-AMA) plays a major role in Amanita phalloides poisoning, showing toxic effects on multi-organs, particularly on the liver and kidneys. Studies have shown a relationship between α-AMA-related injuries and reactive oxygen species.Objectives:We aimed to investigate whether there is renal injury and its relationship with oxidative stress after intraperitoneal injection of α-AMA in mice experimental poisoning models.Materials and Methods:There were 37 male BALB/c laboratory mice treated with α-AMA, according to the study groups: control group (n = 7); low dose (0.2 mg/kg) (n = 10); moderate dose (0.6 mg/kg) (n = 10), and high dose (1 mg/kg) (n = 10). The sample size was detected according to the ethical committee’s decision as well as similar studies in the literature. After a 48-hour follow-up period, all the subjects were sacrificed for pathological and biochemical assays. The study was held in Turkey.Results:α-AMA poisoning in mice results in inflammatory changes and necrosis in renal structures. There were statistically significant differences between the study groups regarding measured levels of catalase, superoxide dismutase, glutathione peroxidase, total antioxidant status (TAS), total oxidant status (TOS) and malonyl dialdehyde in renal homogenates of mice (P < 0.001, P < 0.001, P < 0.001, P < 0.001, P < 0.001, and P = 0.001, respectively). The TOS and TAS measurements helped to eliminate cumbersome analysis of diverse oxidant and antioxidant molecules. The TOS levels in renal homogenate of mice were significantly higher in all the intoxication groups compared to the control group (5.73, 7.02, 7.77, and 9.65 mmol trolox eq/g protein and P = 0.002, P = 0.001, and P = 0.001, respectively). The TAS levels in moderate and high-dose groups were significantly lower than all the other groups treated with α-AMA (0.130, 0.152, 0.065, and 0.087 mmol trolox eq/g protein and P = 0.031, P = 0.001, and P = 0.001, respectively).Conclusions:Our results indicated that α-AMA poisoning in mice led to inflammatory changes and necrosis in renal structures. Biochemical analysis showed a shift in the oxidative/anti-oxidative balance towards the oxidative status.

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Section: Discussionmentioning

confidence: 91%

Alpha-Amanitin Poisoning, Nephrotoxicity and Oxidative Stress: An Experimental Mouse Model

Ergin

Dündar

Kılınç

et al. 2015

Iran Red Crescent Med J

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“…For histopathological evaluation, all kidneys were examined and photographed using light microscopy (Zeiss, Axiphot, Germany) by a pathologist who was blinded to the study groups. Renal injury of the cortex and medulla, including tubular degeneration, tubular dilatation, tubular cell swelling and tubular architectural impairment, was scored semi-quantitatively using three slides from each kidney specimen at ×200 to ×400 magni cation according to the following criteria [28]: normal, 0; involvement of ≤10% of the cortex and medulla, 1; involvement of 11-20% of the cortex and medulla, 2; involvement of 21-30% of the cortex and medulla, 3; involvement of >30% of the cortex and medulla, 4. Mononuclear in ammatory cells in the interstitium were scored as follows: no accumulation, 0; slight accumulation, 1; moderate accumulation, 2; extensive accumulation, 3.…”

Section: Histopathological Assessmentmentioning

confidence: 99%

Carvacrol prevents methotrexate-induced renal oxidative injury and renal damage in rats

Bozkurt¹,

Em²,

Oktayoğlu³

et al. 2014

CIM

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TurkeyCarvacrol prevents methotrexateinduced renal oxidative injury and renal damage in rats AbstractPurpose: e purpose of this study was to investigate the e ect of carvacrol (CAR) on methotrexate (MTX)-induced renal damage in rats.Methods: Twenty-four male rats were equally divided into three groups: group I, control treatment; group II, MTX-treated; and group III, MTX+CAR-treated. A single dose of CAR (73 mg/kg) was administered intraperitoneally to group III on the rst day of the experiment and a single dose of MTX (20 mg/kg) was administered intraperitoneally to groups II and III on the second day of the experiment. Blood samples and kidney tissue were obtained from each animal on day 8 for the measurement of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI). Light microscopy was used for histopathological examination of kidney specimens.Results: MDA, TOS and OSI levels were signi cantly greater in the group receiving MTX alone relative to the control animals, while the TAS level was signi cantly reduced in the MTX group compared with the control group. e administration of CAR was associated with signi cantly decreased MDA, TOS, and OSI levels and increased TAS levels relative to the rats treated with MTX alone. Animals treated with CAR exhibited decreased tubular degeneration and architectural impairment relative to animals treated with MTX alone; however, the di erence in histological scores did not meet the threshold of statistical signi cance. e folic acid antagonist methotrexate (MTX) is used clinically to inhibit the synthesis of purines and pyrimidines [1]. MTX is commonly used at high doses to limit the growth of malignancies, but may also be used at low doses in in ammatory diseases, including psoriasis and rheumatoid arthritis, to inhibit the proliferation of in ammatory leukocytes [2][3][4]. MTX remains an essential component of modern clinical therapy for acute lymphoblastic leukemia and is the primary treatment for malignant gestational trophoblastic disease [5]. In addition to anti-proliferative activity, MTX has antiin ammatory and immunomodulatory properties; however, cytotoxic e ects and other side e ects limit the e cacy of MTX as an anti-in ammatory. Signi cant side e ects of MTX have been described in several organ systems. In particular, MTX has a detrimental e ect on kidney function [6]; however, the mechanism of MTX-induced toxicity remains unclear. More than 90% of MTX is ltered by the kidneys [7] and MTX treatment is known to cause renal failure at high doses [8]. Renal impairment can result in altered metabolism of MTX, delayed drug excretion and, subsequently, systemic toxicity. e toxic e ects of MTX are typically treated through hydration and alkalinization of the patient; however, these methods are insu cient to prevent all instances of MTX toxicity. Reactive oxygen species (ROS) have been implicated in the pathogenesis of MTX-induced renal damage [9,10]. MTX produces free oxygen radicals, resulting in enhanced li...

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“…It has lipophilic properties and easily diffuses through tissues and generates toxic effects in certain organs such as kidney. Protective effect of CAPE was studied against the toxic effect of toluene [68]. Intraperitoneally injected toluene and toluene plus CAPE were investigated in terms of kidney toxicity.…”

Section: Protective Efficacy Of Cape In Kidney Pathologiesmentioning

confidence: 99%

“…By supposing that compounds that act as antioxidants may contribute to the improvement of ASA-mediated renal toxicity, researchers aimed to investigate the protective effects of CAPE against ASA-induced renal oxidative stress used as readouts biochemical parameters and the histopathology of kidney [68]. Rats were given ASA at dose of 50 or 100 mg/kg/day for 5 days via orogastric gavage or ASA together with CAPE at dose of 20 μ g/kg/day for 5 days.…”

Section: Protective Efficacy Of Cape In Kidney Pathologiesmentioning

confidence: 99%

Caffeic Acid Phenethyl Ester as a Protective Agent against Nephrotoxicity and/or Oxidative Kidney Damage: A Detailed Systematic Review

Akyol

Ugurcu

Altuntaş³

et al. 2014

The Scientific World Journal

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Caffeic acid phenethyl ester (CAPE), an active component of propolis, has been attracting the attention of different medical and pharmaceutical disciplines in recent years because of its antioxidant, anti-inflammatory, antiproliferative, cytotoxic, antiviral, antifungal, and antineoplastic properties. One of the most studied organs for the effects of CAPE is the kidney, particularly in the capacity of this ester to decrease the nephrotoxicity induced by several drugs and the oxidative injury after ischemia/reperfusion (I/R). In this review, we summarized and critically evaluated the current knowledge regarding the protective effect of CAPE in nephrotoxicity induced by several special medicines such as cisplatin, doxorubicin, cyclosporine, gentamycin, methotrexate, and other causes leading to oxidative renal injury, namely, I/R models and senility.

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Caffeic Acid Phenethyl Ester Protects Kidneys against Acetylsalicylic Acid Toxicity in Rats

Cited by 7 publications

References 22 publications

Alpha-Amanitin Poisoning, Nephrotoxicity and Oxidative Stress: An Experimental Mouse Model

Alpha-Amanitin Poisoning, Nephrotoxicity and Oxidative Stress: An Experimental Mouse Model

Carvacrol prevents methotrexate-induced renal oxidative injury and renal damage in rats

Caffeic Acid Phenethyl Ester as a Protective Agent against Nephrotoxicity and/or Oxidative Kidney Damage: A Detailed Systematic Review

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