A selenoprotein T-derived peptide protects the heart against ischaemia/reperfusion injury through inhibition of apoptosis and oxidative stress

2018 ◽  
Vol 223 (4) ◽  
pp. e13067 ◽  
Author(s):  
C. Rocca ◽  
L. Boukhzar ◽  
M. C. Granieri ◽  
I. Alsharif ◽  
R. Mazza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Selenoprotein T ◽  
And Oxidative Stress

scholarly journals Protective Effects of GYY4137 on Renal Ischaemia/Reperfusion Injury through Nrf2-Mediated Antioxidant Defence

2021 ◽  
pp. 1-9
Author(s):  
Hongmei Zhao ◽  
Yun Qiu ◽  
Yichen Wu ◽  
Hong Sun ◽  
Sumin Gao
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Nuclear Translocation ◽  
Organ Damage ◽  
Related Factor ◽  
Protective Effects ◽  
Ischaemia Reperfusion Injury ◽  
Renal Ischaemia ◽  
Ischaemia Reperfusion ◽  
Renal Histology

<b><i>Introduction/Aims:</i></b> Hydrogen sulfide (H<sub>2</sub>S) is considered to be the third most important endogenous gasotransmitter in organisms. GYY4137 is a long-acting donor for H<sub>2</sub>S, a gas transmitter that has been shown to prevent multi-organ damage in animal studies. We previously reported the effect of GYY4137 on cardiac ischaemia reperfusion injury (IRI) in diabetic mice. However, the role and mechanism of GYY4137 in renal IRI are poorly understood. The aims of this study were to determine whether GYY4137 can effectively alleviate the injury induced by renal ischaemia reperfusion and to explore its possible mechanism. <b><i>Methods:</i></b> Mice received right nephrectomy and clipping of the left renal pedicle for 45 min. GYY4137 was administered by intraperitoneal injection for 2 consecutive days before the operation. The model of hypoxia/reoxygenation injury was established in HK-2 cells, which were pre-treated with or without GYY4137. Renal histology, function, apoptosis, and oxidative stress were measured. Western blot was used to measure the target ­protein after renal IRI. <b><i>Results:</i></b> The results indicated that GYY4137 had a clear protective effect on renal IRI as reflected by the attenuation of renal dysfunction, renal tubule injury, and apoptosis. Moreover, GYY4137 remarkably reduced renal IRI-induced oxidative stress. GYY4137 significantly elevated the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nrf2) and the expression of antioxidant enzymes regulated by Nrf2, including SOD, HO-1, and NQO-1. <b><i>Conclusions:</i></b> GYY4137 alleviates ischaemia reperfusion-induced renal injury through activating the antioxidant effect mediated by Nrf2 signalling.

The effect of nizatidine on ovarian ischaemia/reperfusion injury in rats

2018 ◽  
Author(s):  
Ilhan Bahri Delibas ◽  
Ibrahim Karaca ◽  
Omer Erkan Yapca ◽  
Metin Ingec ◽  
Serkan Kumbasar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Cardiac Injury ◽  
Leukocyte Infiltration ◽  
Ischaemia Reperfusion Injury ◽  
Ovarian Artery ◽  
Heart Damage ◽  
Ischaemia Reperfusion ◽  
The Right ◽  
And Control

An ischaemia/reperfusion (I/R) injury in an organ can also cause damage to other organs. In this study, the effects of nizatidine were investigated on ovarian I/R injury and subsequent heart damage in rats. Rats were divided into groups; ovarian I/R (IRG), nizatidine 25 mg/kg+ ovarian I/R (NIR), and control (CG) groups. The NIR and IRG groups were given 2 hours of ischaemia followed by 2 hours of reperfusion by applying, and subsequently releasing, a vascular clip to the right ovarian artery. While oxidant levels in the IRG group were higher than NIR and CG groups, antioxidant levels were lower. Necrosis, congested blood vessels, haemorrhage, leukocyte infiltration and oedema were observed in the ovarian and heart tissues of the IRG group. These findings were reduced in the NIR group. Nizatidine suppressed oxidative stress in ovarian and heart tissues and may be useful in prevention of I/R–induced ovarian and cardiac injury.

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