大鼠肝缺血再灌注损伤模型心内过氧化物酶Ⅲ、过氧化氢酶及超氧化物歧化酶的表达变化  

Changes of peroxiredoxin Ⅲ,catalases and superoxide dismutases expression in the heart of rats with hepatic ischemia-reperfusion injury

作　　者：王切[1] 吴琼[2] 王素玲[3] 王磊[1] 

机构地区：[1]河北医科大学解剖学教研室,石家庄050017 [2]河北医科大学第二医院神经内科肌电图室,石家庄050000 [3]河北省血液中心检验科,石家庄050071

出　　处：《解剖学报》2015年第6期832-836,共5页Acta Anatomica Sinica

摘　　要：目的观察大鼠肝缺血再灌注损伤模型心肌组织的氧化应激状态以及抗氧化酶过氧化物酶Ⅲ(PrxⅢ)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)的表达变化。方法 Wistar雄性大鼠12只,随机分为两组。参照Kohli等的方法制造大鼠70%肝缺血再灌注损伤模型,对照组只分离肝蒂,损伤再灌注6h后取血、肝和心。速率法测定血清丙氨酸氨基转移酶(ALT)和乳酸脱氢酶(LDH)活性。光学显微镜观察肝和心的形态学改变。硫代巴比妥酸比色法测定心肌组织丙二醛(MDA)含量,RT-PCR法测定抗氧化酶PrxⅢ、CAT、SOD的mRNA表达水平,Western blotting法测定蛋白水平的表达变化。结果与对照组相比,肝缺血再灌注损伤组大鼠血清ALT活性、LDH活性和心肌MDA的含量均明显升高;HE染色结果显示,肝结构受损明显,但心结构未发现明显改变;心肌组织抗氧化酶PrxⅢ、CAT、SOD的mRNA水平和蛋白水平均明显升高。结论肝缺血再灌注损伤虽未引起心结构的改变,但心肌组织已遭受过氧化损伤;抗氧化酶PrxⅢ、CAT、SOD在此过程中可能发挥了抗氧化应激作用,对心脏具有保护功能。Objective To observe the oxidative stress level of myocardial tissue and the changes of peroxiredoxin Ⅲ （Prx Ⅲ） , 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 Prx Ⅲ, CAT and SOD mRNA in myocardial tissue were evaluated by RT-PCR and protein levels of Prxm, 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.

关 键 词：缺血再灌注损伤 过氧化物酶Ⅲ 过氧化氢酶 超氧化物歧化酶 氧化应激 免疫印迹法 大鼠 

分 类 号：R32[医药卫生—人体解剖和组织胚胎学]