scholarly journals C60 Exposure Augments Cardiac Ischemia/Reperfusion Injury and Coronary Artery Contraction in Sprague Dawley Rats

2014 ◽  
Vol 141 (1) ◽  
pp. 324-324
Keyword(s):  
Coronary Artery ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals C60 Exposure Augments Cardiac Ischemia/Reperfusion Injury and Coronary Artery Contraction in Sprague Dawley Rats

2014 ◽  
Vol 138 (2) ◽  
pp. 365-378 ◽  
Author(s):  
Leslie C. Thompson ◽  
Rakhee N. Urankar ◽  
Nathan A. Holland ◽  
Achini K. Vidanapathirana ◽  
Joshua E. Pitzer ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Glycine Protects the Liver from Reperfusion Injury following Pneumoperitoneum

2018 ◽  
Vol 59 (1-2) ◽  
pp. 91-99 ◽  
Author(s):  
Mohammed Al-Saeedi ◽  
Arash Nickkholgh ◽  
Daniel Schultze ◽  
Christa Flechtenmacher ◽  
Markus Zorn ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Sprague Dawley ◽  
Co2 Pneumoperitoneum ◽  
Hepatic Microcirculation ◽  
Exact Test ◽  
Sprague Dawley Rats ◽  
Latex Beads

Background: Experimental pneumoperitoneum induces ischemia/reperfusion injury (IRI) in the liver, most likely via Kupffer cell (KC)-dependent mechanisms. Glycine has been shown to ameliorate IRI in various animal models. Thus, this study was performed to assess the effects of glycine on the liver after pneumoperitoneum. Materials and Methods: Sprague-Dawley rats (220–250 g in weight) underwent CO2 pneumoperitoneum (12 mm Hg) for 90 min. Some rats received i.v. glycine (1.5 mL, 300 mM) 10 min before pneumoperitoneum. Controls were given the same volume of Ringer’s solution. Transaminases, hepatic microcirculation, and phagocytosis of latex beads indexing both liver injury and KC activation were examined following pneumoperitoneum. Analysis of variance (ANOVA), plus a subsequent t test or χ2 test (or Fisher’s exact test) were carried out as appropriate. Results are presented as mean ± SEM. Results: Glycine significantly decreased lactate dehydrogenase at 1 h and both aspartate aminotransferase and alanine aminotransferase at 2 h after pneumoperitoneum from 477 ± 43, 154 ± 17, and 60 ± 6 U/L in controls to 348 ± 25, 101 ± 11, and 34 ± 3 U/L, respectively (p < 0.05). In parallel, glycine significantly decreased both the rate of permanent adherence of leukocytes to the endothelium by up to 35% and the rate of phagocytosis by > 50% compared to the control group. Conclusion: Glycine decreased IRI after pneumoperitoneum, most likely via KC-dependent mechanisms.

scholarly journals Comparison of ischemic preconditioning and BotulinumA Toxin injection for the prevention of ischemia-reperfusion injury in musculocutaneous flaps

2020 ◽  
Vol 50 (6) ◽  
pp. 1523-1534
Author(s):  
Handan DEREBAŞINLIOĞLU ◽  
Anıl DEMİRÖZ ◽  
Yağmur AYDIN ◽  
Hakan EKMEKÇİ ◽  
Özlem BALCI EKMEKÇİ ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sprague Dawley ◽  
Pedicle Flap ◽  
Musculocutaneous Flaps ◽  
Sprague Dawley Rats ◽  
Significant Difference

Background/aim: The aim of the study was to evaluate the protective effect of Botulinum A toxin injection against ischemia-reperfusion injury.Materials and methods: Thirty-two Sprague-Dawley rats were divided into: control, ischemia-reperfusion, ischemic preconditioning, and botulinum groups. In all groups the musculocutaneous pedicle flap was occluded for 4 h, and then reperfused to induce ischemia-reperfusion injury. Serum and tissue myeloperoxidase (MPO) and nitric oxide (NO) levels were measured at 24 h and at 10 days.Results: Tissue MPO levels did not differ significantly between the ischemic preconditioning and botulinum groups at 24 h but was significantly lower in the botulinum group at 10 days. Tissue NO levels were significantly higher in the ischemic preconditioning group compared to the botulinum group at 24 h and at 10 days. Serum MPO showed no significant difference between these two groups at 24 h but was significantly lower in the ischemic preconditioning group compared to the botulinum group at 10 days. Serum NO levels were not significantly different at 24 h but significantly higher in the botulinum group at 10 days.Conclusion: Findings show that botulinum has a protective effect against the ischemia-reperfusion injury via increased NO and decreased MPO levels in tissue. Based on tissue NO levels, ischemic preconditioning was significantly higher than botulinum.

scholarly journals JAK Inhibition Prevents DNA Damage and Apoptosis in Testicular Ischemia-Reperfusion Injury via Modulation of the ATM/ATR/Chk Pathway

2021 ◽  
Vol 22 (24) ◽  
pp. 13390
Author(s):  
Farah Khashab ◽  
Farah Al-Saleh ◽  
Nora Al-Kandari ◽  
Fatemah Fadel ◽  
May Al-Maghrebi
Keyword(s):  
Dna Damage ◽  
Reperfusion Injury ◽  
Oxidative Dna Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Specific Inhibitor ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Testicular Ischemia ◽  
Ap Sites

Testicular ischemia reperfusion injury (tIRI) causes oxidative stress-induced DNA damage leading to germ cell apoptosis (GCA). The aim of the study is to establish a direct link between JAK2 activation and the DNA damage response (DDR) signaling pathways and their role in tIRI-induced GCA using AG490, a JAK2 specific inhibitor. Male Sprague Dawley rats (n = 36) were divided into three groups: sham, unilateral tIRI and tIRI + AG490 (40 mg/kg). During tIRI, augmentation in the phosphorylation levels of the JAK2/STAT1/STAT3 was measured by immunohistochemistry. Observed spermatogenic arrest was explained by the presence of considerable levels of DSB, AP sites and 8OHdG and activation of caspase 9, caspase 3 and PARP, which were measured by colorimetric assays and TUNEL. The ATM/Chk2/H2AX and ATR/Chk1 pathways were also activated as judged by their increased phosphorylation using Western blot. These observations were all prevented by AG490 inhibition of JAK2 activity. Our findings demonstrate that JAK2 regulates tIRI-induced GCA, oxidative DNA damage and activation of the ATM/Chk2/H2AX and ATR/Chk1 DDR pathways, but the cell made the apoptosis decision despite DDR efforts.

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