Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/72522
Title: Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
Authors: Ying Luo
Nattayaporn Apaijai
Suchan Liao
Chayodom Maneechote
Titikorn Chunchai
Busarin Arunsak
Juthipong Benjanuwattra
Panat Yanpiset
Siriporn C. Chattipakorn
Nipon Chattipakorn
Authors: Ying Luo
Nattayaporn Apaijai
Suchan Liao
Chayodom Maneechote
Titikorn Chunchai
Busarin Arunsak
Juthipong Benjanuwattra
Panat Yanpiset
Siriporn C. Chattipakorn
Nipon Chattipakorn
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Apr-2022
Abstract: Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized that ferroptosis, apoptosis and necroptosis contribute differently to myocardial damage during acute cardiac I/R injury. Rats underwent cardiac I/R or sham operation. I/R-operated rats were divided into 4¬†groups: vehicle, apoptosis (Z-vad), ferroptosis (Fer-1) and necroptosis (Nec-1) inhibition. Rats in each cell death inhibitor group were subdivided into 3 different dose regimens: low, medium and high. Infarct size, left ventricular (LV) function, arrhythmias and molecular mechanism were investigated. Cardiac I/R caused myocardial infarction, LV dysfunction, arrhythmias, mitochondrial dysfunction, mitochondrial dynamic imbalance, inflammation, apoptosis and ferroptosis. Infarct size, LV dysfunction, mitochondrial dysfunction, apoptosis and ferroptosis were all reduced to a similar extent in rats treated with Z-vad (low and medium doses) or Fer-1 (medium and high doses). Fer-1 treatment also reduced mitochondrial dynamic imbalance and inflammation. No evidence of necroptosis was found in association with acute I/R injury, therefore Nec-1 treatment could not be assessed. Apoptosis and ferroptosis, not necroptosis, contributed to myocardial damage in acute I/R injury. Inhibitors of these 2 pathways provided effective cardioprotection in rats with I/R injury though modulation of mitochondrial function and attenuated apoptosis and ferroptosis.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85126781716&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/72522
ISSN: 15821838
Appears in Collections:CMUL: Journal Articles

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