scholarly journals Protective effects of erdosteine, vitamin E, and vitamin C on renal injury induced by the ischemia-reperfusion of the hind limbs in rats

2015 ◽  
Vol 45 ◽  
pp. 33-37 ◽  
Author(s):  
Rana SIRMALI ◽  
Abdullah ARMAĞAN ◽  
Faruk ÖKTEM ◽  
Efkan UZ ◽  
Aynur KIRBAŞ ◽  
...  
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hind Limbs

scholarly journals Protective effects of astaxanthin against ischemia/reperfusion induced renal injury in mice

2015 ◽  
Vol 13 (1) ◽  
pp. 28 ◽  
Author(s):  
Xuefeng Qiu ◽  
Kai Fu ◽  
Xiaozhi Zhao ◽  
Yanting Zhang ◽  
Yimin Yuan ◽  
...  
Keyword(s):  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects

P0522INHIBITING 15-PGDH PREVENTS ISCHEMIC RENAL INJURY BY A PGE2/EP4 SIGNALING PATHWAY MEDIATING VASODILATION, INCREASED RENAL BLOOD FLOW, AND INCREASED ADENOSINE/A2A RECEPTOR

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Byeong Woo KIm ◽  
Sun hee Kim ◽  
Ki beom Bae
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Adenosine A2a Receptor ◽  
Vehicle Group ◽  
Control Group ◽  
Protective Effects ◽  
A2a Receptor ◽  
Adenosine A2a

Abstract Background and Aims We demonstrate the marked activity of SW033291, an inhibitor of 15-hydoxyprostaglandin dehydrogenase (15-PGDH), in preventing acute kidney injury (AKI) in a murine model of ischemia reperfusion injury (IRI). AKI due to ischemic injury represents a significant clinical problem. Prostaglandin E2 (PGE2) is vasodilator in the kidney, but is rapidly degraded in vivo due to catabolism by 15-PGDH. We investigated the potential of SW033291, a potent and specific 15-PGDH inhibitor, as prophylactic treatment for ischemic AKI. Method 10-week aged male C57/BL6 mice were randomly allocated to five groups (n=8 to 15 in each group): the sham-control group, sham-SW033291 group, IRI-vehicle group, IRI-indomethacin group and the IRI-SW033291 group. IRI were induced by clamping bilateral renal artery for 30 min followed by 24 hours of reperfusion. Vehicle, indomethacin, or SW033291 were intraperitoneally administered three times at 1 hour before, immediately after, and 12 hours after IRI. Renal function, histological changes, and renal blood flow were compared and the relevant parameters of oxidative stress and inflammation were detected. Results Prophylactic administration of SW033291 significantly increased renal tissue PGE2 levels and increased post-AKI renal blood flow and renal arteriole area. In parallel, prophylactic SW033291 decreased post-AKI histologic injury score and tubular apoptosis and markedly reduced biomarkers of renal injury that included BUN, creatinine, NGAL and KIM-1. Prophylactic SW033291 also reduced post-AKI induction of proinflammatory cytokines, high mobility group box 1 (HMGB1), and malondialdehyde (MDA). Protective effects of SW033291 were mediated by PGE2 signaling as they could be blocked by pharmacologic inhibition of PGE2 synthesis or of the EP4 type PGE2 receptor. Consistent with activation of PGE2 signaling, SW033291 induced renal levels of both EP4 and of cyclic adenosine monophosphate (cAMP), along with other vasodilatory effectors including AMP, adenosine, and the adenosine A2A receptor (A2A). Protective effects of SW0333291 could largely be achieved with a single prophylactic dose of the drug. Conclusion Inhibiting 15-PGDH may thus represent a novel strategy for prophylaxis of ischemic AKI in multiple clinical settings, including renal transplantation and cardiovascular surgery.

First Report of the Protective Effects of Remote Per- and Postconditioning on Ischemia/Reperfusion-Induced Renal Injury

2011 ◽  
Vol 92 (10) ◽  
pp. e55 ◽  
Author(s):  
Mehri Kadkhodaee ◽  
Behjat Seifi ◽  
Atefeh Najafi ◽  
Zahra Sedaghat
Keyword(s):  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
First Report

scholarly journals Antioxidant modulation of nevirapine induced hepatotoxicity in rats

2015 ◽  
Vol 8 (1) ◽  
pp. 8-14
Author(s):  
Olufunsho Awodele ◽  
Temidayo Popoola ◽  
Kunle Rotimi ◽  
Victor Ikumawoyi ◽  
Wahab Okunowo
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Adverse Effects ◽  
Vitamin C ◽  
Histopathological Examination ◽  
Protective Effects ◽  
Blood Cell Count ◽  
Blood Samples ◽  
Cervical Dislocation ◽  
Related Mortality

AbstractHIV/AIDS related mortality has been dramatically reduced by the advent of antiretroviral therapy (ART). However, ART presents with associated adverse effects. One of such adverse effects is hepatotoxicity observed with nevirapine (NVP) containing ART. Since previous studies showed that NVP hepatotoxicity may be due to oxidative stress via generation of oxidative radicals, this study sought to evaluate the protective effects of antioxidants in alleviating NVP induced hepatotoxicity. Rats were divided into 6 groups with 8 animals per group and received doses of the antioxidants jobelyn (10.7 mg/kg/day), vitamin C (8 mg/kg/day), vitamin E (5 mg/kg/day) and/or NVP (6 mg/kg/day) for 60 days. The animals were sacrificed on day 61 by cervical dislocation, blood samples were collected for biochemical and hematological examination. The liver of the sacrificed animals was weighed and subjected to histopathological examination. There was a statistically significant (p<0.05) elevation in MDA level observed in the NVP group as compared with control. The results further showed non-significant decreases in the levels of MDA in the NVP plus antioxidant groups, except vitamin C, when compared with the NVP alone group. Vitamin E and Vitamin E plus C treated groups showed significantly (p<0.05) higher levels of SOD, CAT and GSH. The results also showed statistically significantly (p<0.05) lower levels of ALT and AST in the antioxidant treated groups There was an observed significantly (p<0.05) higher level of TP and urea in the antioxidant treated rats. A significantly (p<0.05) higher white blood cell count was observed in the antioxidant groups. Histopathological assessment of the liver extracted from the rats showed no visible pathology across the groups. Observations from this study suggest a potentially positive modulatory effect of antioxidants and may be indicative for the inclusion of antioxidants in nevirapine containing ART.

Protective effects of captopril in diabetic rats exposed to ischemia/reperfusion renal injury

2012 ◽  
Vol 65 (2) ◽  
pp. 243-252 ◽  
Author(s):  
Amr A. Fouad ◽  
Abdulruhman S. Al-Mulhim ◽  
Iyad Jresat ◽  
Mohamed A. Morsy
Keyword(s):  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Protective Effects

scholarly journals CCR2 Positive Exosome Released by Mesenchymal Stem Cells Suppresses Macrophage Functions and Alleviates Ischemia/Reperfusion-Induced Renal Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Bing Shen ◽  
Jun Liu ◽  
Fang Zhang ◽  
Yong Wang ◽  
Yan Qin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Renal Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Receptor Proteins ◽  
Injury Repair ◽  
Ccr2 Expression ◽  
Renal Ischemia Reperfusion Injury

Mesenchymal stem cells (MSCs) derived exosomes have been shown to have protective effects on the kidney in ischemia/reperfusion-induced renal injury. However, the key components in the exosomes and their potential mechanisms for the kidney protective effects are not well understood. In our current study, we focused on the abundant proteins in exosomes derived from MSCs (MSC-exo) and found that the C-C motif chemokine receptor-2 (CCR2) was expressed on MSC-exo with a high ability to bind to its ligand CCL2. We also proved that CCR2 high-expressed MSC-exo could reduce the concentration of free CCL2 and suppress its functions to recruit or activate macrophage. Further, knockdown of CCR2 expression on the MSC-exo greatly abolished these effects. Finally, we also found that CCR2 knockdown impaired the protective effects of MSC-exo for the renal ischemia/reperfusion injury in mouse. The results indicate that CCR2 expressed on MSC-exo may play a key role in inflammation regulation and renal injury repair by acting as a decoy to suppress CCL2 activity. Our study may cast new light on understanding the functions of the MSC-exo and these receptor proteins expressed on exosomes.

Intermittent hypobaric hypoxia-induced oxidative stress in rat erythrocytes: protective effects of vitamin E, vitamin C, and carnitine

2007 ◽  
Vol 25 (2) ◽  
pp. 221-231 ◽  
Author(s):  
S. Asha Devi ◽  
R. Vani ◽  
M. V. V. Subramanyam ◽  
Shiva Shankar Reddy ◽  
K. Jeevaratnam
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Vitamin C ◽  
Hypobaric Hypoxia ◽  
Protective Effects ◽  
Rat Erythrocytes ◽  
Intermittent Hypobaric Hypoxia

Protective Effects of Crocin on Hemodynamic Parameters and Infarct Size in Comparison with Vitamin E after Ischemia Reperfusion in Isolated Rat Hearts

Planta Medica ◽  
2014 ◽  
Vol 80 (05) ◽  
pp. 393-398 ◽  
Author(s):  
Mahin Dianat ◽  
Mahdi Esmaeilizadeh ◽  
Mohammad Badavi ◽  
Alireza Samarbafzadeh ◽  
Bahareh Naghizadeh
Keyword(s):  
Vitamin E ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hemodynamic Parameters ◽  
Rat Hearts ◽  
Isolated Rat

Effects of sodium nitrite on ischemia-reperfusion injury in the rat kidney

2006 ◽  
Vol 290 (4) ◽  
pp. F779-F786 ◽  
Author(s):  
Mahesh Basireddy ◽  
T. Scott Isbell ◽  
Xinjun Teng ◽  
Rakesh P. Patel ◽  
Anupam Agarwal
Keyword(s):  
Renal Injury ◽  
Ischemia Reperfusion Injury ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Contralateral Kidney ◽  
Treatment Groups ◽  
Tubular Necrosis

Reactive oxygen and nitrogen species play a key role in the pathophysiology of renal ischemia-reperfusion (I/R) injury. Recent studies have shown that nitrite (NO2−) serves as an endogenous source of nitric oxide (NO), particularly in the presence of hypoxia and acidosis. Nanomolar concentrations of NO2− reduce injury following I/R in the liver and heart in vivo. The purpose of this study was to evaluate the role of NO2− in renal I/R injury. Male Sprague-Dawley rats underwent a unilateral nephrectomy followed by 45 min of ischemia of the contralateral kidney or sham surgery under isoflurane anesthesia. Animals received normal saline, sodium NO2−, or sodium nitrate (NO3−; 1.2 nmol/g body wt ip) at 22.5 min after induction of ischemia or 15 min before ischemia. A separate set of animals received saline, NO2−, or NO3− (0.12, 1.2, or 12 nmol/g body wt iv) 45 min before ischemia. Serum creatinine and blood urea nitrogen were increased following I/R injury but were not significantly different among treatment groups at 24 and 48 h after acute renal injury. Interestingly, NO3− administration appeared to worsen renal injury. Histological scoring for loss of brush border, tubular necrosis, and red blood cell extravasation showed no significant differences among the treatment groups. The results indicate that, contrary to the protective effects of NO2− in I/R injury of the liver and heart, NO2− does not provide protection in renal I/R injury and suggest a unique metabolism of NO2− in the kidney.

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