Protective effects of sevoflurane preconditioning on Oxygen-Glucose Deprivation injury. Role of reactive oxygen species and adenosine triphosphate-regulated potassium channels

2007 ◽  
Vol 24 (Supplement 39) ◽  
pp. 2
Author(s):  
L. Velly ◽  
B. Guillet ◽  
P. Canas ◽  
P. Pisano ◽  
N. Bruder
Keyword(s):  
Reactive Oxygen Species ◽  
Potassium Channels ◽  
Adenosine Triphosphate ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Oxygen Species ◽  
Protective Effects ◽  
Sevoflurane Preconditioning

Anesthetic Preconditioning Improves Adenosine Triphosphate Synthesis and Reduces Reactive Oxygen Species Formation in Mitochondria after Ischemia by a Redox Dependent Mechanism

2003 ◽  
Vol 98 (5) ◽  
pp. 1155-1163 ◽  
Author(s):  
Enis Novalija ◽  
Leo G. Kevin ◽  
Janis T. Eells ◽  
Michele M. Henry ◽  
David F. Stowe
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Function ◽  
Adenosine Triphosphate ◽  
Reactive Oxygen ◽  
Atp Synthesis ◽  
Ros Generation ◽  
Oxygen Species ◽  
Protective Effects ◽  
Anesthetic Preconditioning ◽  
Species Formation

Background Mitochondrial changes that characterize the heart after anesthetic preconditioning (APC) or the mechanisms by which mitochondrial triggering factors lead to protection are unknown. This study hypothesized that generation of reactive oxygen species (ROS) during APC is required to initiate the mitochondrial protective effects, and that APC leads to improved mitochondrial electron transport chain function and cardiac function during reperfusion. Methods Isolated guinea pig hearts were subject to 30 min ischemia and 120 min reperfusion. Prior to ischemia hearts were either untreated (I/R), or treated with sevoflurane (APC), in the presence or absence of the ROS scavenger tiron (TIR), or the superoxide dismutase mimetic MnTBAP (TBAP). Intracellular ROS were measured by spectrofluorometry using the fluorescent probe dihydroethidium (DHE). In another series of experiments, using the same protocol, hearts were reperfused for only 5 min and removed for measurement of adenosine triphosphate (ATP) synthesis by luciferin-luciferase luminometry and ROS generation by dichlorohydro-fluorescein (DCF) fluorescence in isolated mitochondria. Results The APC improved cardiac function and reduced infarction. Tiron or MnTBAP abrogated the protection afforded by APC. Mitochondrial ATP synthesis was decreased by 70 +/- 3% after IR alone, by only 7 +/- 3% after APC, by 69 +/- 2% after APC+TIR, and by 71 +/- 3% after APC + TBAP. Mitochondrial ROS formation (DCF) increased by 48 +/- 3% after IR alone, by 0 +/- 2% after APC, by 43 +/- 4% after APC + TIR, and by 46 +/- 3% after APC + TBAP. ROS generation (DHE) was increased in I/R group at 5 and 120 min reperfusion. This was attenuated by APC but this protective effect was abrogated in APC + TIR and APC + TBAP groups. Conclusions The results indicate that ROS are central both in triggering and mediating APC, and that the mitochondrion is the target for these changes.

scholarly journals Protective Effect ofScutellaria litwinowiiExtract on Serum/Glucose-Deprived Cultured PC12 Cells and Determining the Role of Reactive Oxygen Species

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Maryam Afsharzadeh ◽  
Zahra Tayarani-Najaran ◽  
Aryo Zare ◽  
Seyed Hadi Mousavi
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pc12 Cells ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Serum Glucose ◽  
Oxygen Species ◽  
Species Production

Considering the wide, positive reporting of the role of reactive oxygen species in ischemic brain injury, searching for antioxidant drugs within herbal remedies is logical. In this study, the protective effects ofScutellaria litwinowiiBornm. & Sint. on cell viability and reactive oxygen species production in cultured PC12 cells were investigated under serum/glucose-deprivation-induced cell death. After cells were seeded overnight, they were then deprived of serum/glucose for 24 h. Cells were treated with different concentrations ofS. litwinowiiextract (7.75–250 μg/mL). Cell viability was quantitated by MTT assay, and intracellular reactive oxygen species production was measured by flow cytometry. Serum/glucose-deprivation induced significant cell death after 24 h (P< 0.001). Treatment withS. litwinowii(7.75–250 μg/mL) reduced serum/glucose deprivation-induced cytotoxicity in PC12 cells after 24 h. A significant increase in intracellular reactive oxygen species production was seen following serum/glucose deprivation (P< 0.001).S. litwinowii(62 and 125 μg/mL,P< 0.01) treatment reversed the increased reactive oxygen species production following ischemic insult. This demonstrates thatS. litwinowiiextract protects PC12 cells against serum/glucose-deprivation-induced cell death by antioxidant mechanisms, which indicates the potential therapeutic application ofS. litwinowiiin managing cerebral ischemic and neurodegenerative disorders.

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