scholarly journals The Protective Effects of Alpha-Lipoic Acid and Coenzyme Q10Combination on Ovarian Ischemia-Reperfusion Injury: An Experimental Study

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Ahmet Ali Tuncer ◽  
Mehmet Fatih Bozkurt ◽  
Tulay Koken ◽  
Nurhan Dogan ◽  
Mine Kanat Pektaş ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Lipoic Acid ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ovarian Tissue ◽  
Coenzyme Q ◽  
Alpha Lipoic Acid ◽  
Oxide Synthase

Objective. This study aims to evaluate whether alpha-lipoic acid and/or coenzyme Q10can protect the prepubertal ovarian tissue from ischemia-reperfusion injury in an experimental rat model of ovarian torsion.Materials and Methods. Forty-two female preadolescent Wistar-Albino rats were divided into 6 equal groups randomly. The sham group had laparotomy without torsion; the other groups had torsion/detorsion procedure. After undergoing torsion, group 2 received saline, group 3 received olive oil, group 4 received alpha-lipoic acid, group 5 received coenzyme Q10, and group 6 received both alpha-lipoic acid and coenzyme Q10orally. The oxidant-antioxidant statuses of these groups were compared using biochemical measurement of oxidized/reduced glutathione, glutathione peroxidase and malondialdehyde, pathological evaluation of damage and apoptosis within the ovarian tissue, and immunohistochemical assessment of nitric oxide synthase.Results. The left ovaries of the alpha-lipoic acid + coenzyme Q10group had significantly lower apoptosis scores and significantly higher nitric oxide synthase content than the left ovaries of the control groups. The alpha-lipoic acid + coenzyme Q10group had significantly higher glutathione peroxidase levels and serum malondialdehyde concentrations than the sham group.Conclusions. The combination of alpha-lipoic acid and coenzyme Q10has beneficial effects on oxidative stress induced by ischemia-reperfusion injury related to ovarian torsion.

scholarly journals Inhibition of inducible nitric oxide synthase reduces renal ischemia/reperfusion injury

2002 ◽  
Vol 61 (3) ◽  
pp. 862-871 ◽  
Author(s):  
Prabal K. Chatterjee ◽  
Nimesh S.A. Patel ◽  
Espen O. Kvale ◽  
Salvatore Cuzzocrea ◽  
Paul A.J. Brown ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Reperfusion Injury ◽  
Inducible Nitric Oxide Synthase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals ERK phosphorylation mediates sildenafil-induced myocardial protection against ischemia-reperfusion injury in mice

2009 ◽  
Vol 296 (5) ◽  
pp. H1236-H1243 ◽  
Author(s):  
Anindita Das ◽  
Fadi N. Salloum ◽  
Lei Xi ◽  
Yuan J. Rao ◽  
Rakesh C. Kukreja
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Global Ischemia ◽  
Erk Phosphorylation ◽  
Gsk 3Β ◽  
Oxide Synthase

Sildenafil, a selective inhibitor of phosphodiesterase type 5, induces powerful protection against myocardial ischemia-reperfusion injury through activation of cGMP-dependent protein kinase (PKG). We further hypothesized that PKG-dependent activation of survival kinase ERK may play a causative role in sildenafil-induced cardioprotection via induction of endothelial nitric oxide synthase (eNOS)/inducible nitric oxide synthase (iNOS) and Bcl-2. Our results show that acute intracoronary infusion of sildenafil in Langendorff isolated mouse hearts before global ischemia-reperfusion significantly reduced myocardial infarct size (from 29.4 ± 2.4% to 15.9 ± 3.0%; P < 0.05). Cotreatment with ERK inhibitor PD98059 abrogated sildenafil-induced protection (31.8 ± 4.4%). To further evaluate the role of ERK in delayed cardioprotection, mice were treated with sildenafil (ip) 24 h before global ischemia-reperfusion. PD98059 was administered (ip) 30 min before sildenafil treatment. Infarct size was reduced from 27.6 ± 3.3% in controls to 7.1 ± 1.5% in sildenafil-treated mice ( P < 0.05). The delayed protective effect of sildenafil was also abolished by PD98059 (22.5 ± 2.3%). Western blots revealed that sildenafil significantly increased phosphorylation of ERK1/2 and GSK-3β and induced iNOS, eNOS, Bcl-2, and PKG activity in the heart 24 h after treatment. PD98059 inhibited the enhanced expression of iNOS, eNOS, and Bcl-2 and the phosphorylation of GSK-3β. PD98059 had no effect on the sildenafil-induced activation of PKG. We conclude that these studies provide first direct evidence that PKG-dependent ERK phosphorylation is indispensable for the induction of eNOS/iNOS and Bcl-2 and the resulting cardioprotection by sildenafil.

Protective role of nitric oxide synthase against ischemia-reperfusion injury in guinea pig myocardial mitochondria

1999 ◽  
Vol 380 (1) ◽  
pp. 37-48 ◽  
Author(s):  
Yoshihiro Hotta ◽  
Hidetsugu Otsuka-Murakami ◽  
Michiko Fujita ◽  
Junichi Nakagawa ◽  
Michio Yajima ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Guinea Pig ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Myocardial Mitochondria ◽  
Oxide Synthase
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