The effects of polymicrobial sepsis with diabetes mellitus on kidney tissues in ovariectomized rats

Uyanik, Abdullah; Ünal, Deniz; Uyanık, Metin; Halıcı, Zekai; Odabaşoğlu, Fehmi; Altunkaynak, Zuhal; Çadırcı, Elif; Keleş, Mustafa; Gündoğdu, Cemal; Süleyman, Halis; Bayır, Yasin; Albayrak, Mevlüt; Ünal, Bünyami

doi:10.3109/08860221003759478

Cited by 23 publications

(10 citation statements)

References 49 publications

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“…Mortality increased gradually with the puncture size, from 27% with a 22-gauge needle to 95% with the blade incision during a week of observation [38]. In addition, in our previous studies we observed mortality within 12-20 h after sepsis induction with a 12-gauge needle [39][40][41][42]. However, in studies performed with 21-and 22-gauge needles, mortality was not as common [38,43,44].…”

Section: Sepsis Modelmentioning

confidence: 80%

“…ROS have been assumed to play a role in the induction of many proinflammatory cytokines and mediators important in producing the acute inflammatory responses associated with sepsis [12]. In our previous studies we determined that kidney, heart, lung and liver tissue exhibited oxidative stress in septic rats [40][41][42]. The proinflammatory effects of ROS include endothelial damage, formation of chemotactic factors, neutrophil reinforcement, cytokine release and mitochondrial injury [14][15][16], which all contribute to free radical overload and to oxidant-antioxidant imbalance.…”

Section: Discussionmentioning

confidence: 99%

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Sildenafil treatment attenuates lung and kidney injury due to overproduction of oxidant activity in a rat model of sepsis: a biochemical and histopathological study

Çadırcı¹,

Halıcı²,

Odabaşoğlu

et al. 2011

Clinical and Experimental Immunology

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SummarySepsis is a systemic inflammatory response to infection and a major cause of morbidity and mortality. Sildenafil (SLD) is a selective and potent inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase PDE5. We aimed to investigate the protective effects of sildenafil on caecal ligation and puncture (CLP)-induced sepsis in rats. Four groups of rats were used, each composed of 10 rats: (i) 10 mg/kg SLD-treated CLP group; (ii) 20 mg/kg SLD-treated CLP group; (iii) CLP group; and (iv) sham-operated control group. A CLP polymicrobial sepsis model was applied to the rats. All groups were killed 16 h later, and lung, kidney and blood samples were analysed histopathologically and biochemically. Sildenafil increased glutathione (GSH) and decreased the activation of myeloperoxidase (MPO) and of lipid peroxidase (LPO) and levels of superoxide dismutase (SOD) in the septic rats. We observed a significant decrease in LPO and MPO and a decrease in SOD activity in the sildenafil-treated CLP rats compared with the sham group. In addition, 20 mg/kg sildenafil treatment in the sham-operated rats improved the biochemical status of lungs and kidneys. Histopathological analysis revealed significant differences in inflammation scores between the sepsis group and the other groups, except the CLP + sildenafil 10 mg/kg group. The CLP + sildenafil 20 mg/kg group had the lowest inflammation score. Sildenafil treatment decreased the serum tumour necrosis factor (TNF)-a level when compared to the CLP group. Our results indicate that sildenafil is a highly protective agent in preventing lung and kidney damage caused by CLPinduced sepsis via maintenance of the oxidant-anti-oxidant status and decrease in the level of TNF-a.

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Section: Sepsis Modelmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Sildenafil treatment attenuates lung and kidney injury due to overproduction of oxidant activity in a rat model of sepsis: a biochemical and histopathological study

Çadırcı¹,

Halıcı²,

Odabaşoğlu

et al. 2011

Clinical and Experimental Immunology

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“…TNF-α provokes neutrophil-mediated tissue injury by acting on endothelial cells and neutrophils. A primary role for TNF-α in sepsis is also suggested by several studies conducted on cell lines, animal models, and human beings [15,31,32,33,34,35,36]. TNF-α activates IL-6, which is an important mediator in septic shock and a marker of proinflammatory cytokine activation, and is also defined as an early predictor of organ dysfunction.…”

Section: Discussionmentioning

confidence: 95%

The Effects of Montelukast on Antioxidant Enzymes and Proinflammatory Cytokines on the Heart, Liver, Lungs, and Kidneys in a Rat Model of Cecal Ligation and Puncture–Induced Sepsis

Coşkun

Yiğiter

Oral

et al. 2011

The Scientific World JOURNAL

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We investigated the potential protective effects of montelukast (MLK) on cecal ligation and puncture (CLP)–induced tissue injury in vital organs — liver, heart, kidneys, and especially lungs — through inhibition of the proinflammatory cytokine response and the generation of reactive oxygen species (ROS) in rats. The rat groups were (1) a 10-mg/kg MLK-treated CLP group; (2) a 20-mg/kg MLK-treated CLP group; (3) a 20-mg/kg MLK-treated, sham-operated group; (4) a CLP control group; and (5) a sham-operated control group. MLK treatment significantly decreased proinflammatory (tumor necrosis factor-alpha, interleukin-6) cytokine levels following CLP. The lipid peroxide level increased in the lung, heart, liver, and kidney tissues after CLP-induced sepsis, and myeloperoxidase activity increased in the lung, heart, and liver tissues. MLK attenuated this elevation in all tissues except the kidney, dose dependently. The glutathione levels and superoxide dismutase activity were significantly increased in the lung, liver, and kidney tissues after MLK treatment. MLK treatment after CLP also potentially reduced mortality. The lung and kidney tissues were the most protected by MLK under sepsis conditions. We can suggest that MLK reverses the systemic inflammatory reaction to polymicrobial sepsis and thereby reduces multiple organ failure.

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“…All these studies and our findings suggest an increased iNOS expression during diabetes-induced brain damage, and bosentan treatment decreased iNOS expression as a protective mechanism against this damage. Likewise, it was shown that oxidative stress increased in many organs, dependent on diabetes [54,55]. A previous study showed the superoxide scavenger effect of the superoxide dismutase enzyme in cerebral arterioles dependent on type 1 diabetes [56].…”

Section: Discussionmentioning

confidence: 99%

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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The effects of polymicrobial sepsis with diabetes mellitus on kidney tissues in ovariectomized rats

Cited by 23 publications

References 49 publications

Sildenafil treatment attenuates lung and kidney injury due to overproduction of oxidant activity in a rat model of sepsis: a biochemical and histopathological study

Sildenafil treatment attenuates lung and kidney injury due to overproduction of oxidant activity in a rat model of sepsis: a biochemical and histopathological study

The Effects of Montelukast on Antioxidant Enzymes and Proinflammatory Cytokines on the Heart, Liver, Lungs, and Kidneys in a Rat Model of Cecal Ligation and Puncture–Induced Sepsis

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

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