Protective Effects of Selenium on Aflatoxin B1-induced Mitochondrial Permeability Transition, DNA Damage, and Histological Alterations in Duckling Liver

2014 ◽  
Vol 163 (1-2) ◽  
pp. 162-168 ◽  
Author(s):  
Dayou Shi ◽  
Shenquan Liao ◽  
Shining Guo ◽  
Hua Li ◽  
Meimei Yang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Aflatoxin B1 ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Protective Effects ◽  
Mitochondrial Permeability ◽  
Histological Alterations

scholarly journals Morphine Postconditioning Protects Against Reperfusion Injury: the Role of Protein Kinase C-Epsilon, Extracellular Signal-Regulated Kinase 1/2 and Mitochondrial Permeability Transition Pores

2016 ◽  
Vol 39 (5) ◽  
pp. 1930-1940 ◽  
Author(s):  
Zuolei Chen ◽  
Donat R. Spahn ◽  
Xuewei Zhang ◽  
Yingzhi Liu ◽  
Haichen Chu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Permeability Transition ◽  
Protective Effects ◽  
Mitochondrial Permeability ◽  
Mptp Opening ◽  
Extracellular Signal ◽  
Rat Hearts ◽  
Cyt C

Background/Aims: The purpose of this study was to investigate the implications of protein kinase C-epsilon (PKCε), Extracellular Signal-regulated Kinase 1/2 (ERK1/2) and mitochondrial permeability transition pore (mPTP) in myocardial protection induced by morphine postconditioning (MpostC). Methods: The isolated rat hearts were randomly assigned into one of eight groups. Hearts in time control (TC) group were constantly perfused for 105min. Hearts in ischemia-reperfusion (I/R) group were subjected to 45 min of ischemia followed by 1 h of reperfusion. MpostC was induced by 10 min of morphine administration at the onset of reperfusion. εV1-2 (an inhibitor of PKCε) and PD (an inhibitor of ERK1/2) was administered with or without morphine during the first 10 min of reperfusion following the 45 min of ischemia. I/R injury was assessed by functional parameters, creatine kinase-MB (CK-MB) release and infarct size (IS/AAR). Additional hearts were excised at 20 min following reperfusion to detect the membrane-specific translocation of PKCε, ERK1/2 phosphorylation, mitochondrial permeability transition (MPT) and cytochrome C (Cyt-c) release. Results: MpostC markedly reduced infarct size (IS/AAR), CK-MB release, and improved cardiac function recovery. However, these protective effects were partly abolished in the presence of εV1-2 or PD. Compared to TC group, the membrane translocation of PKCε, ERK1/2 phosphorylation, mPTP opening, and Cyt-c release were significantly increased in I/R hearts. MpostC further increased the membrane translocation of PKCε and ERK1/2 phosphorylation, and significantly inhibited mPTP opening and Cyt-c release. However, those protective effects induced by MpostC were abolished by εV1-2 or PD, which, used alone, showed no influence on reperfusion injury. Conclusions: These findings suggest that MpostC protects isolated rat hearts against ischemia-reperfusion injury via activating PKCε-ERK1/2 pathway and inhibiting mPTP opening.

Novel bisindolylmaleimide derivative inhibits mitochondrial permeability transition pore and protects the heart from reperfusion injury

2007 ◽  
Vol 85 (10) ◽  
pp. 979-985 ◽  
Author(s):  
Rajesh Gopalrao Katare ◽  
Zou Zhitian ◽  
Mikiko Sodeoka ◽  
Shiro Sasaguri
Keyword(s):  
Reperfusion Injury ◽  
Left Coronary Artery ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Protective Effects ◽  
Mitochondrial Permeability

Despite major advances in treating patients with coronary heart disease, reperfusion injury is still considered to be a major problem, especially in surgical settings. Here, we demonstrate the protective effects of a novel bisindolylmaleimide derivative, MS1 (2-[1-(3-aminopropyl)indol-3-yl]-3-(indol-3-yl)-N-methylmaleimide), against reperfusion injury of the heart. After anesthesia and artificial ventilation, Wistar rats were subjected to 30 min of left coronary artery occlusion followed by 120 min of reperfusion with or without treating the rats with MS1 (2.25 μmol·L–1·kg–1) before left coronary artery occlusion. Compared with the untreated hearts, MS1 treatment significantly reduced myocardial infarct size (35.1% ± 3% vs. 75.5% ± 5%, p < 0.001), reduced prevalence of apoptotic cells (2.6% ± 0.5% vs. 12.2% ± 2.1%, p < 0.001), prevented mitochondrial swelling and cytochrome c release, inhibited downregulation of antiapoptotic protein Bcl-2 expression, and suppressed caspase-3 activation. In contrast, pretreatment with atractyloside, a mitochondrial permeability transition pore opener, abolished the protective effects of MS1. In conclusion, MS1 inhibits pathologic opening of permeability transition pores and protects the heart against reperfusion injury and pathologic apoptosis.

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