α-Bisabolol abrogates isoproterenol-induced myocardial infarction by inhibiting mitochondrial dysfunction and intrinsic pathway of apoptosis in rats.
Calcium overload
Intrinsic apoptotic pathway
Isoproterenol
Mitochondrial dysfunction
Oxidative stress
α-Bisabolol
Journal
Molecular and cellular biochemistry
ISSN: 1573-4919
Titre abrégé: Mol Cell Biochem
Pays: Netherlands
ID NLM: 0364456
Informations de publication
Date de publication:
Mar 2019
Mar 2019
Historique:
received:
26
04
2018
accepted:
21
08
2018
pubmed:
31
8
2018
medline:
28
2
2019
entrez:
31
8
2018
Statut:
ppublish
Résumé
Mitochondrial dysfunction plays crucial role in the pathologenesis of myocardial infarction (MI). The present study evaluated the protective effect of α-bisabolol against isoproterenol (ISO)-induced mitochondrial dysfunction and apoptosis in rats. Male albino Wistar rats were pre- and co-treated with intraperitoneal injection of α-bisabolol (25 mg/kg body weight) daily for 10 days. To induce experimental MI, ISO (85 mg/kg body weight) was injected subcutaneously to the rats at an interval of 24 h for 2 days (9th and 10th day). ISO-induced MI was indicated by the decreased activities of heart creatine kinase and lactate dehydrogenase in rats. ISO administration also enhanced the concentrations of heart mitochondrial lipid peroxidation products and decreased the activities/concentrations of mitochondrial antioxidants, Kreb's cycle dehydrogenases and mitochondrial electron transport chain complexes I, II + III and IV in rats. Furthermore, ISO triggers calcium overload and ATP depletion in the rat's heart mitochondria followed by the mitochondrial cytochrome-C release and the activation of intrinsic pathway of apoptosis by upregulating the myocardial pro-apoptotic Bax, P
Identifiants
pubmed: 30159796
doi: 10.1007/s11010-018-3434-5
pii: 10.1007/s11010-018-3434-5
doi:
Substances chimiques
Mitochondrial Proteins
0
Monocyclic Sesquiterpenes
0
Muscle Proteins
0
Sesquiterpenes
0
bisabolol
24WE03BX2T
Isoproterenol
L628TT009W
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
89-102Subventions
Organisme : University Program for Advanced Research (UPAR)
ID : 31M195
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