Postconditioning has been verified to provide cardioprotection and is associated with the state of mitochondrial permeability transition pore. However, there are a few limitations with clinical use of classic postconditioning; therefore, the purpose of this investigation was to study whether inhibition of mitochondrial permeability transition pore opening with cyclosporine A also provided cardioprotection. Langendorff-perfused Sprague-Dawley rat hearts were perfused for 20 minutes with Krebs-Henseleit buffer followed by 30 minutes of crystalloid cardioplegia and 60 minutes of reperfusion. Control hearts (Con group) were reperfused with Krebs-Henseleit buffer. Postconditioning hearts (Ipo group) were with six cycles of 10 seconds reocclusion separated by 10 seconds perfusion before reperfusion. Cyclosporine A postconditioning hearts (CsA group) were reperfused with Krebs-Henseleit buffer containing 0.8 μmol/L cyclosporine A at first 5 minutes of reperfusion. Compared with Con group, myocardial performance was better preserved in CsA group. Mitochondrial outer membrane integrity was preserved, with less cytosolic diffusion of cytochrome C (p < 0.05) and less frequency of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick end labeling-positive myocytes in Ipo and CsA group (p < 0.05). Postconditioning prevented apoptosis-related mitochondrial permeabilization and dysfunction after cardioplegic arrest. Cyclosporine A postconditioning had a better effect than classic postconditioning in myocardial performance.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1097/MAT.0b013e31820bffc1 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
RIPK3 activation of CaMKII triggers mitochondrial apoptosis in NIBV-infected renal tubular epithelial cells.
Vet Microbiol
January 2025
Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, China. Electronic address:
The purpose of this study was to investigate whether RIPK3-mediated programmed cell death can promote the replication and transmission of renal infectious bronchitis virus in renal tubular epithelial cells. Primary renal tubular epithelial cells were extracted from 1 to 7 day old Hy-Line Brown chicks, cultured in vitro by type I collagenase digestion, and infected with 1MOI SX9 strain. Cell samples were collected at 12 hpi, 24 hpi, 36 hpi and 48 hpi for experimental exploration.
View Article and Find Full Text PDFAdenine nucleotide translocator and ATP synthase cooperate in mediating the mitochondrial permeability transition.
J Physiol
January 2025
Department of Biomedical Sciences, University of Padova, Padova, Italy.
The permeability transition (PT) is a permeability increase of the mitochondrial inner membrane causing mitochondrial swelling in response to matrix Ca. The PT is mediated by regulated channel(s), the PT pore(s) (PTP), which can be generated by at least two components, adenine nucleotide translocator (ANT) and ATP synthase. Whether these provide independent permeation pathways remains to be established.
View Article and Find Full Text PDFValidation of a Coarse-Grained Martini 3 Model for Molecular Oxygen.
J Chem Theory Comput
January 2025
IBiTech - BioMMedA Group, Ghent University, Corneel Heymanslaan 10, Entrance 98, 9000 Gent, Belgium.
Molecular oxygen (O) is essential for life, and continuous effort has been made to understand its pathways in cellular respiration with all-atom (AA) molecular dynamics (MD) simulations of, e.g., membrane permeation or binding to proteins.
View Article and Find Full Text PDFMicroenvironment-induced programmable nanotherapeutics restore mitochondrial dysfunction for the amelioration of non-alcoholic fatty liver disease.
Acta Biomater
January 2025
Key Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; Shandong Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong, 250021, China; Shandong Engineering Laboratory of Prevention and Control for Endocrine and Metabolic Diseases, Jinan, Shandong, 250021, China. Electronic address:
Nonalcoholic fatty liver disease (NAFLD) is a metabolic liver disorder with severe complications. Mitochondrial dysfunction due to over-opening of the mitochondrial permeability transition pore (mPTP) in liver cells plays a central role in the development and progression of NAFLD. Restoring mitochondrial function is a promising strategy for NAFLD therapy.
View Article and Find Full Text PDFRole of AIM2 and cGAS-STING signaling in high fat high carbohydrate diet-induced gut dysbiosis associated neurodegeneration.
Life Sci
January 2025
Department of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research, Chunilal Bhawan, 168, Maniktala Main Rd, Kolkata, West Bengal 700054, India. Electronic address:
Aims: Gut dysbiosis modulates CNS complications and cognitive decline through the gut-brain axis. The study aims to investigate the molecular mechanisms involved in gut dysbiosis-associated cognitive changes and the potential effects of probiotics in high fat-high carbohydrate diet-induced gut dysbiosis-associated neurodegeneration.
Materials And Methods: We used high fat, high-carbohydrate diet (HFHCD) and high-fat diet (HFD) to induce gut dysbiosis-associated neurodegeneration in C57BL/6 mice.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!