Renal Ischemia/Reperfusion Injury in Diabetic Rats: The Role of Local Ischemic Preconditioning

Özbılgın, Şule; Özkardeşler, Sevda; Akan, Mert; Boztaş, Nilay; Özbilgin, Mücahit; Ergur, Bekir Uğur; Derici, Serhan; Güneli, Mehmet Ensari; Meseri, Reci

doi:10.1155/2016/8580475

Cited by 27 publications

(17 citation statements)

References 30 publications

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“…injection with 2 % ( w/w ) pentobarbital sodium (3.0 ml/kg bw) [28, 29]. Then they were equally randomized into four groups: (1) STZ-induced diabetic rat (DM group), wherein the diabetic rats were treated only with separating the bilateral renal arteries and veins; (2) DM + renal I/R injury (I/R group), wherein the diabetic rats were treated with ischemia by clamping the bilateral renal arteries and veins for 45 min and subsequent 2-h reperfusion; (3) DM + renal I/R injury + R-568 group (R group), wherein the R-568 (an agonist of CaSR, 2.5 mg/kg bw, dissolved in 10% dimethyl sulphoxide) was administered by i.p.…”

Section: Methodsmentioning

confidence: 99%

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Hu¹,

Tong²,

Xu³

et al. 2018

Kidney Blood Press Res

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Background/Aims: Renal ischemia/reperfusion (I/R) injury (RI/RI) is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations at its onset, which can result in inflammation, abnormal lipid metabolism, the production of reactive oxygen species (ROS), and nitroso-redox imbalance. The calcium-sensing receptor (CaSR) is a G-protein coupled receptor, however, the functional involvement of CaSR in diabetic RI/ RI remains unclear. The present study was intended to investigate the role of CaSR on RI/RI in diabetes mellitus (DM). Methods: The bilateral renal arteries and veins of streptozotocin (STZ)-induced diabetic rats were subjected to 45-min ischemia followed by 2-h reperfusion with or without R-568 (agonist of CaSR) and NPS-2143 (antagonist of CaSR) at the beginning of I/R procedure. DM without renal I/R rats served as control group. The expressions of CaSR, calmodulin (CaM), and p47phox in the renal tissue were analyzed by qRT-PCR and Western blot. The renal pathomorphology, renal function, oxidative stress, inflammatory response, and calcium disorder were evaluated by detection of a series of indices by hematoxylin-eosin (HE) staining, transmission electron microscope (TEM), commercial kits, enzyme-linked immunosorbent assay (ELISA), and spectrophotofluorometry, respectively. Results: Results showed that the expressions of CaSR, CaM, and p47phox in I/R group were significantly up-regulated as compared with those in DM group, which were accompanied by renal tissue injury, increased calcium, oxidative stress, inflammation, and nitroso-redox imbalance. Conclusion: These results suggest that activation of CaSR is involved in the induction of damage of renal tubular epithelial cell during diabetic RI/RI, resulting in lipid peroxidation, inflammatory response, nitroso-redox imbalance, and apoptosis.

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Section: Methodsmentioning

confidence: 99%

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Hu¹,

Tong²,

Xu³

et al. 2018

Kidney Blood Press Res

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“…It is known that acute renal failure is significantly associated with renal iri, but the pathological mechanisms of renal iri are complex (5). Most of the recent studies on iri primarily focus on aspects including apoptosis and necrosis of renal tubular epithelial cells, free radical-induced injury, calcium overload, the obstacles of energy metabolism, adhesion molecules and cell factors (6,7). once iri has occurred, the prognosis of the patients is significantly affected.…”

Section: Introductionmentioning

confidence: 99%

Role of prostaglandin E2 receptor 4 in the modulation of apoptosis and mitophagy during ischemia/reperfusion injury in the kidney

et al. 2019

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The mechanisms by which prostaglandin e2 receptor 4 (eP4) protects against renal ischemia-reperfusion (i/r) injury (iri) remain to be fully elucidated. in the present study, the protective effects of eP4 signaling on renal mitochondria and against renal iri, as well as the underlying mechanisms, were investigated. a rat model of renal iri was established. The right kidney was separated without damaging the artery clip, and the renal blood perfusion was then restored after 60 min. one group of animals was treated with eP4 agonists prior to i/r. The mitochondrial mass, the copy number of mitochondrial (mt)dna, adenosine triphosphate (aTP) production and mitochondrial autophagy were analyzed. it was identified that renal iri reduced the mitochondrial mass, decreased the mtdna copy number and inhibited aTP production. The loss of renal mitochondria was attributed to the excessive mitochondrial autophagy induced by renal iri. Pre-treatment with eP4 agonist inhibited excessive mitochondrial autophagy, the loss of mitochondria and maintained and the energy imbalance within the cells. it was indicated that renal iri causes excessive mitochondrial autophagy, which is one of the important causes of renal dysfunction.

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“…Ischemic preconditioning (IPC) is a potent protective strategy in which a brief occlusion of ischemia and reperfusion results in tolerance to subsequent ischemia-reperfusion injury 8,9 . It has been demonstrated in multiple tissues and organs including the heart, liver, small intestine, and renal tissues [10][11][12][13] . Low-energy shock waves have been used in many fields to reduce the damage induced by tissue ischemia or to improve recovery after ischemia.…”

Section: ■ Introductionmentioning

confidence: 99%

Low-energy shock wave preconditioning reduces renal ischemic reperfusion injury caused by renal artery occlusion

Xue

Chen

et al. 2017

Acta Cir. Bras.

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. Acquisition, analysis and interpretation of data; statistical analysis. AbstractPurpose: To evaluate whether low energy shock wave preconditioning could reduce renal ischemic reperfusion injury caused by renal artery occlusion. Methods: The right kidneys of 64 male Sprague Dawley rats were removed to establish an isolated kidney model. The rats were then divided into four treatment groups: Group 1 was the sham treatment group; Group 2, received only low-energy (12 kv, 1 Hz, 200 times) shock wave preconditioning; Group 3 received the same low-energy shock wave preconditioning as Group 2, and then the left renal artery was occluded for 45 minutes; and Group 4 had the left renal artery occluded for 45 minutes. At 24 hours and one-week time points after reperfusion, serum inducible nitric oxide synthase (iNOS), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), creatinine (Cr), and cystatin C (Cys C) levels were measured, malondialdehyde (MDA) in kidney tissue was detected, and changes in nephric morphology were evaluated by light and electron microscopy. Results: Twenty-four hours after reperfusion, serum iNOS, NGAL, Cr, Cys C, and MDA levels in Group 3 were significantly lower than those in Group 4; light and electron microscopy showed that the renal tissue injury in Group 3 was significantly lighter than that in Group 4. One week after reperfusion, serum NGAL, KIM-1, and Cys C levels in Group 3 were significantly lower than those in Group 4. Conclusion: Low-energy shock wave preconditioning can reduce renal ischemic reperfusion injury caused by renal artery occlusion in an isolated kidney rat model.

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Renal Ischemia/Reperfusion Injury in Diabetic Rats: The Role of Local Ischemic Preconditioning

Cited by 27 publications

References 30 publications

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Role of prostaglandin E2 receptor 4 in the modulation of apoptosis and mitophagy during ischemia/reperfusion injury in the kidney

Low-energy shock wave preconditioning reduces renal ischemic reperfusion injury caused by renal artery occlusion

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