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Antiapoptotic Cardioprotective Effect of Hypothermia Treatment Against Oxidative Stress Injuries
Author(s) -
Huang ChienHua,
Chen HueiWen,
Tsai MinShan,
Hsu ChiungYuan,
Peng RenHow,
Wang TzungDau,
Chang WeiTien,
Chen WenJone
Publication year - 2009
Publication title -
academic emergency medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.221
H-Index - 124
eISSN - 1553-2712
pISSN - 1069-6563
DOI - 10.1111/j.1553-2712.2009.00495.x
Subject(s) - tunel assay , oxidative stress , medicine , hypothermia , reactive oxygen species , apoptosis , terminal deoxynucleotidyl transferase , annexin , pharmacology , hydrogen peroxide , andrology , mitochondrion , endocrinology , anesthesia , staining , biochemistry , chemistry , pathology , immunohistochemistry
Objectives: The effect of hypothermia on cardiomyocyte injury induced by oxidative stress remains unclear. The authors investigated the effects of hypothermia on apoptosis and mitochondrial dysfunction in cardiomyocytes exposed to oxidative stress. Methods: Cardiomyocytes (H9c2) derived from embryonic rat heart cell culture were exposed to either normothermic (37°C) or hypothermic (31°C) environments before undergoing oxidative stress via treatment with hydrogen peroxide (H 2 O 2 ). The degree of apoptosis was determined by annexin V and terminal deoxynucleotidyl transferase (TUNEL) staining. The amount of reactive oxygen species (ROS) was compared after H 2 O 2 exposure between normo‐ and hypothermic‐pretreated groups. Mitochondrial dysfunction in both groups was measured by differential reductase activity and transmembrane potential (ΔΨm). Results: Hydrogen peroxide induced significant apoptosis in both normothermic and hypothermic cardiomyocytes. Hypothermia ameliorated apoptosis as demonstrated by decreased annexin V staining (33 ± 1% vs. 49 ± 4%; p < 0.05) and TUNEL staining (27 ± 17% vs. 80 ±25%; p < 0.01). The amount of intracellular ROS increased after H 2 O 2 treatment and was higher in the hypothermic group than that in the normothermic group (237.9 ± 31.0% vs. 146.6 ± 20.6%; p < 0.05). In the hypothermic group, compared with the normothermic group, after H 2 O 2 treatment mitochondrial reductase activity was greater (72.0 ± 17.9% vs. 27.0 ± 13.3%; p < 0.01) and the mitochondria ΔΨm was higher (101.0 ± 22.6% vs. 69.7 ± 12.9%; p < 0.05). Pretreatment of cardiomyocytes with the antioxidant ascorbic acid diminished the hypothermia‐induced increase in intracellular ROS and prevented the beneficial effects of hypothermia on apoptosis and mitochondrial function. Conclusions: Hypothermia at 31°C can protect cardiomyocytes against oxidative stress–induced injury by decreasing apoptosis and mitochondrial dysfunction through intracellular ROS‐dependent pathways.