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   <subfield code="a">10.1007/s10620-011-1607-0</subfield>
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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s10620-011-1607-0</subfield>
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   <subfield code="a">Mitochondrial Dependent Apoptosis: Ameliorative Effect of Flunarizine on Ischemia-Reperfusion of Celiac Artery-Induced Gastric Lesions in the Rat</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Arunachalam Muthuraman, Muthusamy Ramesh, Ashish Chauhan]</subfield>
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   <subfield code="a">Objectives: Ischemia-reperfusion is a major event for induction of cellular apoptosis. Apoptosis is due to the activation of death receptor and/or mitochondrial pathways. Mitochondrial permeability transition pore opening is the cause of apoptosis. In our present study, we tried to evaluate the role of flunarizine in ischemia and reperfusion of celiac artery-induced gastric lesion in the rat. Methods: The therapeutic potential of flunarizine was assessed by measuring the changes in gastric lesion index, biomarker (i.e., thiobarbituric acid reactive substance, reduced glutathione, superoxide dismutase, myeloperoxidase, and total calcium and protein content), and mitochondrial damage (i.e., adenosine triphosphate and deoxyribonucleic acid fragmentation content) in ischemia and reperfusion-induced gastric lesion model. Results: Medium and higher doses of flunarizine produced a significant (P&lt;0.05) ameliorative effect which was observed from the assessment of all the above-mentioned parameters (i.e., increase in reduced glutathione, superoxide dismutase and decrease in thiobarbituric acid reactive substance, myeloperoxidase, and total calcium content). Similar results were also obtained from omeprazole and cyclosporine. In the pre-treated group, deoxyribonucleic acid fragmentation pattern has also indicated that a mitochondria-associated anti-apoptotic effect of flunarizine was responsible to prevent the ischemia and reperfusion of celiac artery-induced gastric lesion. Conclusion: The gastroprotective effect of flunarizine may be produced due to its inactivation potential of mitochondrial permeability transition pore opening associated with anti-oxidative, calcium regulation along with its anti-apoptotic effect.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2011</subfield>
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   <subfield code="a">Apoptosis</subfield>
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   <subfield code="a">Cyclosporine A</subfield>
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   <subfield code="a">Flunarizine</subfield>
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   <subfield code="a">Free radical</subfield>
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   <subfield code="a">Ischemia-reperfusion</subfield>
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   <subfield code="a">Muthuraman</subfield>
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   <subfield code="u">Rayat Institute of Pharmacy, Nawanshahr District, Near Railmajra, 144533, Ropar, Punjab, India</subfield>
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   <subfield code="a">Ramesh</subfield>
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   <subfield code="u">National Institute of Pharmaceutical Education and Research (NIPER), Mohali, Punjab, India</subfield>
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   <subfield code="u">Rayat Institute of Pharmacy, Nawanshahr District, Near Railmajra, 144533, Ropar, Punjab, India</subfield>
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   <subfield code="t">Digestive Diseases and Sciences</subfield>
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   <subfield code="g">56/8(2011-08-01), 2244-2251</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
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