scholarly journals Protection of Liver as a Remote Organ after Renal Ischemia-Reperfusion Injury by Renal Ischemic Postconditioning

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Behjat Seifi ◽  
Mehri Kadkhodaee ◽  
Atefeh Najafi ◽  
Atefeh Mahmoudi
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Sham Group ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Ischemic Postconditioning ◽  
Male Rats ◽  
Sham Operation ◽  
Sod Activity ◽  
Remote Organ

This study was designed to investigate the protective effects of local renal ischemic postconditioning (POC) on liver damage after renal ischemia-reperfusion (IR) injury. Male rats were divided into three groups  (n=8). They underwent a right nephrectomy before induction of 45 minutes of left kidney ischemia or sham operation. POC was performed by four cycles of 10 seconds of ischemia and 10 seconds of reperfusion just at the beginning of 24 hours of reperfusion. Then blood and liver samples were collected to measure serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and liver oxidative stress parameters including superoxide dismutase (SOD) activity and malondialdehyde (MDA) level. Renal IR caused a significant increase in liver functional indices as demonstrated by increased serum AST and ALT compared to sham group. These parameters reduced significantly in POC group compared to IR group. Liver MDA levels increased and SOD activity decreased in IR group compared to sham group. Induction of POC reduced the elevated liver MDA levels and increased the reduced liver SOD activity. These results revealed that renal IR injury causes liver damage as a remote organ and POC protects liver from renal IR injury by a modification in the hepatic oxidative stress status.

scholarly journals Pancreatic Injury Secondary to Renal Ischemia/Reperfusion (I/R) Injury: Possible Role of Oxidative Stress

2014 ◽  
pp. 47-55 ◽  
Author(s):  
A. M. HUSSEIN ◽  
A. ABD-ELKHABIR ◽  
A. ABOZAHRA ◽  
A. BAIOMY ◽  
S. A. ASHAMALLAH ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Serum Creatinine ◽  
Sham Group ◽  
Serum Amylase ◽  
Ischemia Reperfusion ◽  
Fasting Blood Glucose ◽  
Renal Ischemia ◽  
Male Adult ◽  
Midline Laparotomy

Recent studies demonstrated remote effects of renal ischemia/reperfusion (I/R) injury on some organs such as brain, liver, and lungs. We investigated the effects of renal I-R injury on function, histology and oxidative stress state of pancreas. Twenty -four male adult Sprague-Dawley rats were divided equally into 2 groups; sham group: rats underwent midline laparotomy and dissection of renal pedicles without renal ischemia, and ischemic group: rats underwent bilateral renal ischemia for 45 min. Renal functions (serum creatinine and BUN), pancreatic functions (serum amylase, lipase and insulin) and fasting blood glucose were measured at 2 h, 1 day, 3 days and 7 days after ischemia. Also, pancreatic histology and malondialdehyde (MDA), catalase and reduced glutathione (GSH) were examined at 2 h and 7 days after ischemia. The ischemic rats showed significant increase in serum creatinine and BUN with significant increase in serum amylase and lipase at 2 h, 1 day and 3 days after ischemia. Blood glucose and fasting insulin showed no significant change apart from significant increase in insulin in sham group at 1 day after ischemia. Pancreas isolated from ischemic rats showed significant increase in histopathological damage score and significant increase in MDA and catalase enzyme with decrease in GSH. In conclusion, bilateral renal ischemia for 45 min caused significant impairment of pancreatic functions and histology. This might be due to deficiency of antioxidant and increased lipid peroxidations in pancreatic tissues.

Intermedin protects against renal ischemia-reperfusion injury by inhibition of oxidative stress

2013 ◽  
Vol 304 (1) ◽  
pp. F112-F119 ◽  
Author(s):  
Xi Qiao ◽  
Rong-Shan Li ◽  
Hong Li ◽  
Guo-Zhen Zhu ◽  
Xiao-Guang Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Critical Role ◽  
Renal Ischemia ◽  
Kidney Cells ◽  
Sod Activity ◽  
Renal Ischemia Reperfusion Injury

Reactive oxygen species (ROS) play a critical role in renal ischemia-reperfusion injury (IRI). Intermedin (IMD) reportedly protected against myocardial IRI via its antioxidant effects; however, its protective role in renal IRI has not been investigated. We overexpressed IMD in rat kidneys and examined how the kidneys respond to renal IRI. Eukaryotic expression plasmid encoding the rat IMD gene or control empty vector was transfected into the left kidney using an ultrasound-microbubble-mediated delivery system. This method yielded high expression of IMD in kidney cells. Renal IRI was induced by clamping the left renal artery followed by reperfusion. In response to IRI, overexpression of IMD in the kidney significantly improved renal function and pathology compared with the kidney transfected with control plasmid. We investigated the mechanisms by which IMD protects against renal IRI. We examined renal superoxide dismutase (SOD) activity and malondialdehyde (MDA) content and found SOD activity was significantly increased, while MDA level was markedly decreased in kidneys transfected with IMD, suggesting ROS production and oxidative stress were reduced by IMD overexpression. We also measured myeloperoxidase (MPO) activity, tubular cell apoptosis, and the expression of intercellular adhesion molecule-1 (ICAM-1), P-selectin, and endothelin-1 (ET-1) in the kidney. Renal MPO activity and the expression of ICAM-1, P-selectin, and ET-1 stimulated by IRI were significantly inhibited by IMD overexpression. Moreover, IMD overexpression prevented kidney cells from apoptosis caused by IRI. Our results demonstrate that overexpression of IMD in the kidney protects against renal IRI, apparently by reducing oxidative stress, consequently suppressing inflammation and vasoconstrictor production and apoptosis.

scholarly journals Determination of Dynamic Plasma Thiol -disulfide Homeostasis with a Novel Technique in Intestinal Ischemia Reperfusion Injury

2021 ◽  
Vol 2 (3) ◽  
pp. 55-59
Author(s):  
Ersin Gürkan Dumlu ◽  
Mehmet Tokaç ◽  
Mustafa Özsoy ◽  
İbrahim Kılınç ◽  
Nazmiye Dinçer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intestinal Ischemia ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Albino Rats ◽  
Sham Operation ◽  
Total Thiol ◽  
Ischemia Group ◽  
Intestinal Ischemia Reperfusion

Introduction: Intestinal ischemia/reperfusion (I/R) is a serious life-threatening clinical case. Overproduction of reactive oxygen species (ROS) associated with oxidative stress plays a key role in I/R pathophysiology. Objective: The aim of this study is to evaluate dynamic thiol / disulfide hemostasis in intestinal I/R in rats. Materials and Methods: 24 Winstar albino rats were divided into 3 groups (8 animals in each group: (1) sham (operation without ischemia), (2) ischemia (90 minutes ischemia), (3) ischemia/reperfusion (after ischemia for 30 minutes reperfusion for 60 minutes). At the end of the process, liver samples were evaluated pathologically. Also, in plasma samples, native thiol, disulphide and total thiol levels were measured. Results: Native thiol levels in ischemia and I/R group were found to be significantly lower compared to the sham group (P<0.001). Disulfide levels in Ischemia group were found to be significantly higher compared to the sham group (P< 0.05). Disulfide / native thiol levels in ischemia and I/R group were found to be significantly higher compared to the sham group (P < 0.05). Disulfide / total thiol levels in both ischemia and I/R group were found to be significantly higher compared to the sham group (P< 0.05). Conclusion: Balance of dynamic thiol/disulfide is a quite suitable indicator for evaluating oxidative stress which occurs as a result of intestinal I/R. As a result, measurement of dynamic thiol/disulfide balance with Erel method is fully automated and practical for evaluating oxidative environment which is formed with ischemia reperfusion.

Molecular Dissection of Renal Ischemia-Reperfusion: Oxidative Stress and Cellular Events

2016 ◽  
Vol 23 (19) ◽  
pp. 1965-1980 ◽  
Author(s):  
Branislav Rovcanin ◽  
Branislava Medic ◽  
Gordana Kocic ◽  
Tatjana Cebovic ◽  
Marko Ristic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Molecular Dissection ◽  
Cellular Events

Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death

2021 ◽  
pp. 153537022199520
Author(s):  
Nanees F El-Malkey ◽  
Amira E Alsemeh ◽  
Wesam MR Ashour ◽  
Nancy H Hassan ◽  
Husam M Edrees
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Beclin 1 ◽  
Male Rats ◽  
Fetuin A ◽  
Intestinal Ischemia Reperfusion ◽  
And Oxidative Stress

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

scholarly journals The protective effects of pomegranate extracts against renal ischemia-reperfusion injury in male rats

2014 ◽  
Vol 6 (1) ◽  
pp. 46 ◽  
Author(s):  
AhmetA Sancaktutar ◽  
MehmetN Bodakci ◽  
NamıkK Hatipoglu ◽  
Kemal Basarılı ◽  
Haluk Soylemez ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Male Rats ◽  
Protective Effects ◽  
Renal Ischemia Reperfusion Injury

scholarly journals The Preventive Effects of Diminazene Aceturate in Renal Ischemia/Reperfusion Injury in Male and Female Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Maryam Malek ◽  
Mehdi Nematbakhsh
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Female Rats ◽  
Male Rats ◽  
Converting Enzyme ◽  
Diminazene Aceturate ◽  
Male And Female ◽  
Male And Female Rats

Background. Angiotensin-converting enzyme 2/angiotensin (1-7)/Mas receptor (ACE2/Ang-1-7/MasR) appears to counteract most of the deleterious actions of angiotensin-converting enzyme/angiotensin II/angiotensin II receptor 1 (ACE/Ang II/AT1R) in renal ischemia/reperfusion (I/R) injury but ACE2 activity and its levels are sexually dimorphic in the kidney. This study was designed to evaluate the effects of activation endogenous ACE2 using the diminazene aceturate (DIZE) in renal I/R injury in male and female rats.Methods. 36 Wistar rats were divided into two groups of male and female and each group distinct to three subgroups (n=6). I/R group was subjected to 45 min of bilateral ischemia and 24 h of reperfusion, while treatment group received DIZE (15 mg/kg/day) for three days before the induction of I/R. The other group was assigned as the sham-operated group.Results. DIZE treatment in male rats caused a significant decrease in blood urea nitrogen (BUN), creatinine, liver functional indices, serum malondialdehyde (MDA), and increase kidney nitrite levels (P<0.05), and in female rats a significant increase in creatinine and decrease serum nitrite levels compared to the I/R group (P<0.05).Conclusions. DIZE may protect the male kidney from renal I/RI through antioxidant activity and elevation of circulating nitrite level.

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