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Changes of peroxiredoxin Ⅲ, catalases and superoxide dismutases expression in the heart of rats with hepatic ischemia-reperfusion injury
WANG Qie WU Qiong WANG Su-ling WANG Lei*
Acta Anatomica Sinica ›› 2015, Vol. 46 ›› Issue (6) : 832-836.
Changes of peroxiredoxin Ⅲ, catalases and superoxide dismutases expression in the heart of rats with hepatic ischemia-reperfusion injury
Objective To observe the oxidative stress level of myocardial tissue and the changes of peroxiredoxin Ⅲ（PrxⅢ）, catalases（CAT）andsuperoxide dismutases（SOD）expression in hepatic ischemia-reperfusion injury (HIRI)model of rats. Methods Totally 12 male Wistar rats were randomly divided into two groups. The hepatic ischemia-reperfusion injury model of rats was established based on Kohli V’s methods. Only was the hepatic pedicle separated in control group. The serum, liver and heart were taken followed by 6h reperfusion. The activities of serum alanine transaminase（ALT）and lactate dehydrogenase（LDH）LDH were detected by the rate method. The morphological changes of liver and heart were observed with HE staining. The malondialdehyde (MDA) content in myocardial tissue was determined by Thiobarbituric acid colorimetric method. The expressions of PrxⅢ, CAT and SOD mRNA in myocardial tissue were evaluated by RT-PCR and protein levels of PrxⅢ, CAT and SOD were estimated by Western blotting. Results Compared with the control group, the activity of ALT and LDH in serum, MDA content in HIRI group were significantly increased. Structures of liver tissue of HIRI model were severely impaired according to the results of HE staining, but that of the heart were not changed. The mRNA and protein level of PrxⅢ, CAT and SOD in myocardial tissue of HIRI model were increased markedly. Conclusion HIRI can not cause the change of heart structures, but the myocardial tissue suffers from peroxidative damage. The antioxidase PrxⅢ, CAT and SOD may play an important role in the antioxidation effect during the process and protect the myocardial tissue.
Ischemia-reperfusion injury / Peroxiredoxin Ⅲ / Superoxide dismutase / Catalase / Oxidative stress / Western blotting / Rat
［1］Li J, Li RJ, Lü GY,et al. The mechanisms and strategies to protect from hepatic ischemia-reperfusion injury［J］. Eur Rev Med Pharmacol Sci,2015,19(11):2036-2047.
［2］Liu B, Ma ZY, Wu G,et al. Butyrate protects rats from hepatic ischemia/reperfusion injury［J］. Int J Clin Exp Med, 2015,8(4):5406-5413.
［3］Katsumi H, Fukui K, Sato K,et al. Pharmacokinetics and preventive effects of platinum nanoparticles as reactive oxygen species scavengers on hepatic ischemia/reperfusion injury in mice［J］. Metallomics,2014,6(5):1050-1056.
［4］Jaeschke H, Woolbright BL. Current strategies to minimize hepatic ischemia-reperfusion injury by targeting reactive oxygen species［J］. Transplant Rev (Orlando),2012,26(2):103-114.
［5］Elias-Miró M, Jiménez-Castro MB, Rodés J,et al. Current knowledge on oxidative stress in hepatic ischemia/reperfusion［J］. Free Radic Res,2013,47(8):555-568.
［6］Tsutsui H, Kinugawa S, Matsushima S. Oxidative stress and heart failure［J］. Am J Physiol Heart Circ Physiol, 2011, 301(6):H2181-H2190.
［7］Kohli V, Selzner M, Madden JF, et al. Endothelial cell and hepatocyte deaths occur by apoptosis after ischemia-reperfusion injury in the rat liver［J］. Transplantation,1999,67(8):1099-1105.
［8］Gracia-Sancho J, Casillas-Ramírez A, Peralta C. Molecular pathways in protecting the liver from ischaemia/reperfusion injury:a 2015 update［J］. Clin Sci (Lond), 2015,129(4):345-362.
［9］Pan S, Liu L, Pan H,et al. Protective effects of hydroxytyrosol on liver ischemia/reperfusion injury in mice［J］. Mol Nutr Food Res,2013, 57(7):1218-1227.
［10］Jin G, Qiu G, Wu D, et al. Allogeneic bone marrow-derived mesenchymal stem cells attenuate hepatic ischemia-reperfusion injury by suppressing oxidative stress and inhibiting apoptosis in rats［J］. Int J Mol Med, 2013, 31(6):1395-1401.
［11］Zhang LH, Wang Q, Liu Zh, et al. Expression of peroxiredoxin I-thioredoxin, superoxide dismutases and catalases mRNA in hepatic ischemia-reperfusion injury of rats［J］. Acta Anatomica Sinica, 2013,44(4):550-553. (in Chinese)
张丽华,王切,刘钊,等.过氧化物还原酶I-硫氧还蛋白、超氧化物歧化酶及过氧化氢酶在大鼠肝脏缺血再灌注损伤中的表达变化［J］. 解剖学报,2013,44(4):550-553.
［12］Kwiecien S, Konturek PC, Sliwowski Z, et al. Interaction between selective cyclooxygenase inhibitors and capsaicin-sensitive afferent sensory nerves in pathogenesis of stressinduced gastric lesions. Role of oxidative stress［J］. Physiol Pharmacol, 2012,63(2):143-151.
［13］Derouiche F, B?le-Feysot C, Na?mi D, et al. Hyperhomocysteinemia-induced oxidative stress differentially alters proteasome composition and activities in heart and aorta［J］. Biochem Biophys Res Commun,2014,452(3):740-745.
［14］Gao S, Oh YB, Park BM, et al. Urotensin II protects ischemic reperfusion injury of hearts through ROS and antioxidant pathway［J］. Peptides,2012,36(2):199-205.
［15］Borchi E, Bargelli V, Stillitano F, et al. Enhanced ROS production by NADPH oxidase is correlated to changes in antioxidant enzyme activity in humanheart failure［J］. Biochim Biophys Acta,2010,1802(3):331-338.
［16］Whitaker HC, Patel D, Howat WJ, et al. Peroxiredoxin-3 is overexpressed in prostate cancer and promotes cancer cell survival by protecting cells from oxidative stress［J］. Br J Cancer,2013,109(4):983-993.
［17］Haynes AC, Qian J, Reisz JA, et al. Molecular basis for the resistance of human mitochondrial 2-Cys peroxiredoxin 3 to hyperoxidation［J］. J Biol Chem,2013,288(41):29714-29723.
［18］Araki M, Nanri H, Ejima K, et al. Antioxidant function of the mitochondrial protein SP-22 in the cardiovascular system［J］. J Biol Chem,1999,274(4):2271-2278.
［19］Matsushima S, Ide T,Yamato M, et al. Overexpression of mitochondrial peroxiredoxin-3 prevents left ventricular remodeling and failure after myocardial infarction in mice［J］. Circulation,2006,113(14):1779-1786.
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