ArticleDigestive diseases and sciences2011
Mitochondrial dependent apoptosis: ameliorative effect of flunarizine on ischemia-reperfusion of celiac artery-induced gastric lesions in the rat.
Article in Digestive diseases and sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Flunarizine attenuates ischemia-reperfusion-induced ovarian injury in rats.Journal of ovarian research · 2026Article
- Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer.Oxidative medicine and cellular longevity · 2020Review
- Antiulcer Activity and Potential Mechanism of Action of the Leaves ofOxidative medicine and cellular longevity · 2018Article
- Reperfusion injury and reactive oxygen species: The evolution of a concept.Redox biology · 2015Review
- Geraniol-a flavoring agent with multifunctional effects in protecting the gastric and duodenal mucosa.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- Study on the antiulcer effects of Veronicastrum axillare on gastric ulcer in rats induced by ethanol based on tumor necrosis factor-α (TNF-α) and endothelin-1 (ET-1).Asian Pacific journal of tropical biomedicine · 2013Article
- Neuroprotective effect of gadolinium: a stretch-activated calcium channel blocker in mouse model of ischemia-reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Therapeutic potential of 7,8-dimethoxycoumarin on cisplatin- and ischemia/reperfusion injury-induced acute renal failure in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
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3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectivesIschemia-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.
methodsThe 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.
resultsMedium and higher doses of flunarizine produced a significant (P<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.
conclusionThe 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.
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