Blockade of endothelin receptors with bosentan limits ischaemia/reperfusion-induced injury in rat ovaries

Şengül, Özlem; Ferah, Irmak; Polat, Beyzagül; Halıcı, Zekai; Bayır, Yasin; Yılmaz, Mehmet Emin; Kılıç, Nergiz; Keleş, Osman Nuri

doi:10.1016/j.ejogrb.2013.06.040

Cited by 20 publications

(22 citation statements)

References 49 publications

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“…This finding demonstrates that an I/R injury induced increased MDA release, considered to be a good indicator of lipid peroxidation. In our study, MDA data in the I/R group were in compliance with previous studies performed with an I/R model . Although many studies have been performed related to ovarian I/R injury, as far as we know, this study is the first to investigate the impact of CVD treatment on an ovarian I/R model.…”

Section: Discussionsupporting

confidence: 84%

Effects of carvedilol on an ischemia/reperfusion model: Biochemical, histopathological and immunohistochemical evaluation

Özsoy

Nursal

Arıcı

et al. 2016

J of Obstet and Gynaecol

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Section: Discussionsupporting

confidence: 84%

Effects of carvedilol on an ischemia/reperfusion model: Biochemical, histopathological and immunohistochemical evaluation

Özsoy

Nursal

Arıcı

et al. 2016

J of Obstet and Gynaecol

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“…The SOD activity of our study decreased in the diabetic rats. Other studies showed that the SOD activity increased dependent on diabetes [69] and bosentan administration improved antioxidant status [62,63]. In summary, the bosentan application improved all antioxidant parameters in our study.…”

Section: Discussionsupporting

confidence: 73%

“…In one clinical study, serum MDA levels and endothelin-1 levels were found to be high in patients with type 2 diabetes [61]. Furthermore, it was determined that in acetaminophen-induced hepatotoxicity and over torsion-induced ischaemia-reperfusion injury, increased MDA levels were decreased by bosentan application, and there was histopathological improvement in the related tissues [62,63]. These studies support increased MDA levels during diabetes and protective effects of bosentan.…”

Section: Discussionmentioning

confidence: 83%

Does Bosentan Protect Diabetic Brain Alterations in Rats? The Role of Endothelin‐1 in the Diabetic Brain

Demir

Çadırcı

Akpınar

et al. 2014

Basic Clin Pharma Tox

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Diabetes mellitus (DM) is a major problem all over the world, affecting more people in recent years. Individuals with diabetes are more prone to disease than non-diabetics, especially vascular complications. The aim of this study was to examine the roles of the endothelin (ET)-1 in brain damage formed in a streptozocin (STZ)-induced diabetes model, and the effect of bosentan, which is the non-specific ET1 receptor blocker in the prevention of the diabetes-induced brain damage. To examine the effects of bosentan (50 mg/kg and 100 mg/kg) in this study, the rats were given the drug for 3 months. The rats were divided into four groups: the sham group (n = 10), the diabetic control group (n = 10), the group of diabetic rats given bosentan 50 mg/ kg (n = 10) and the group of diabetic rats given bosentan 100 mg/kg (n = 10). Diabetes was induced in the rats by STZ (60 mg/kg i.p.). On day 91, all rats were killed. Brain tissues of the rats were measured by molecular, biochemical and histopathological methods. Antioxidant levels in the therapy groups were observed as quite near to the values in the healthy group. In this study, while the brain eNOS levels in the diabetic groups decreased, the ET1 and iNOS levels were found to be increased. However, in the diabetes group, hippocampus and cerebellum, pericellular oedema and a number of neuronal cytoretraction were increased in neuropiles, whereas these results were decreased in the therapy group. Based on all of these results, ET1 will not be ignored in diabetes-induced cerebral complications.Diabetes mellitus (DM) is a severe disease which eventually results in death. During diabetes mellitus, tissues cannot uptake glucose and very severe complications such as nephropathy, retinopathy, neuropathy and peripheral vascular complications occur [1]. Many new mechanisms have been suggested during the formation and progress of these complications. There are studies in many areas, from inflammation to cellular membrane disorders, of the mechanisms of diabetesinduced complications [1][2][3]. There are also many studies on the receptors which are responsible for the formation of diabetes and diabetes-induced complications in relation to our topic: angiotensin receptors, urotensin receptors, glucagon-like peptide 1 receptors and peroxisome proliferator-activated receptora [4,5].Previous studies have shown the importance of angiotensin in diabetes-induced liver damage [6,7], and there are many recent studies showing that endothelin-1 receptors play important roles in diabetes. One study showed that cell proliferation and, at the same time, ET1 production increased in type 2 diabetes [8,9]. Diabetes-related, clinical and experimental studies showed that ET1 plasma levels increased [10,11]. A study by Mastumoto et al. showed that the expression of both ET1 and the receptors increased in the streptozotocin (STZ)-induced diabetes model [12]. In another study, giving endothelin-1 to individuals with insulin resistance reduced endothelin-1-induced vasodilatation [13]. ET1 levels w...

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“…Recent studies have reported that proinflammatory interleukin 1 beta (IL-1β) is increased in ovarian tissues subjected to IR. 9 On the other hand, excess oxidative stress kills cells, either by necrosis or by apoptosis. 10,11 In many models of apoptosis, alterations in the redox status of the cell to a more oxidizing environment occurs prior to the final phase of caspase activation.…”

Section: Introductionmentioning

confidence: 99%

Effect of Kineret® on ovarian ischemia reperfusion injury in a rat model

Naykı

Cetin

et al. 2016

J of Obstet and Gynaecol

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Blockade of endothelin receptors with bosentan limits ischaemia/reperfusion-induced injury in rat ovaries

Cited by 20 publications

References 49 publications

Effects of carvedilol on an ischemia/reperfusion model: Biochemical, histopathological and immunohistochemical evaluation

Effects of carvedilol on an ischemia/reperfusion model: Biochemical, histopathological and immunohistochemical evaluation

Does Bosentan Protect Diabetic Brain Alterations in Rats? The Role of Endothelin‐1 in the Diabetic Brain

Effect of Kineret® on ovarian ischemia reperfusion injury in a rat model

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