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Progressive Thermal Preconditioning Efficiently Attenuates Rat Cardiac Ischemia/Reperfusion Injury
Author(s) -
Chen YuehHsi
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1278.1
Subject(s) - ischemia , reperfusion injury , cardiac function curve , oxidative stress , medicine , apoptosis , microcirculation , autophagy , cardioprotection , ischemic preconditioning , pharmacology , endocrinology , anesthesia , chemistry , cardiology , biochemistry , heart failure
Progressive thermal preconditioning (PTP) to whole‐body hyperthermia is the protective effects on oxidative stress, which may have cardioprotective properties against ischemia/reperfusion (I/R) injury from efficiently diminish apoptosis and autophagy. We divided Male Wistar rats into non‐PTP control group, 72 h after a single or three consecutive cycles of PTP in a 42°C water bath (1–72, and 3–72 groups). Anesthetized male Wistar rats were subjected to 60 min of regional ischemia followed by 240 min of reperfusion. We measured cardiac O 2 −. amounts in vivo in response to left anterior descending coronary artery ligation for 1 h and reperfusion for 4 h. Cardiac function and injury was determined by microcirculation, electrocardiogram, infarct size and ventricular contractile function. PTP‐induced protective effects on oxidative stress, apoptosis‐and autophagy‐related mechanisms were examined by western blot and immunohistochemistry. Coronary arterial ischemia/reperfusion depressed cardiac microcirculation, induced S‐T segment elevation and increased infarct size in non‐PTP and PTP rats. Ischemia/reperfusion enhanced cardiac O 2 − . levels, erythrocyte and leukocytes infiltration, cytosolic cytochrome C release and the decreased mitochondrial Bcl‐2 expression. Cardiac injury increased Bax/Bcl‐2 ratio, cleaved caspase 3 expression and poly‐(ADP‐ribose)‐polymerase fragments leading to apoptosis formation, and promoted LC3‐II expression resulting in autophagy formation. PTP treatment elevated HSP70 and Bcl‐2 in the rat heart especially in the 3–72 group. PTP treatment significantly restored cardiac microcirculation and ventricular contractile function, and decreased inflammation, oxidative stress, apoptosis, autophagy and infarct size. PTP significantly reduces cardiac ischemia/reperfusion injury via the upregulating antioxidant, anti‐inflammatory, anti‐apoptotic and anti‐autophagic mechanisms.