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The effects of antioxidants and nitric oxide modulators on hepatic ischemic-reperfusion injury in rats.

机译:抗氧化剂和一氧化氮调节剂对大鼠肝脏缺血再灌注损伤的影响。

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摘要

Ischemic-reperfusion injury (IRI) is thought to be caused by oxygen radicals. Nitric oxide (NO) also has been thought to play a key role in IRI. This experiment was designed to evaluate the effects of antioxidants and NO supplement on hepatic IRI. Male Sprague-Dawley rats were divided into five groups: a sham operation group, a group with IRI, and three groups with vitamin C combined with vitamin E (VC&VE), L-arginine and N(G)-nitro-L-arginine (NNLA) injected after IRI. IRI was induced by clamping of the porta hepatis for 30 minutes and then by declamping. To prevent mesenteric blood congestion, a porto-systemic shunt had been made four weeks before the portal clamping. Biochemical assays of TNF-alpha level and NO2- level in the blood, malondialdehyde level, catalase activity and NO synthase activity in the liver tissue were performed. The results were as follows: IRI increased the malondialdehyde level and exhausted the catalase activity remarkably. VC&VE lowered the malondialdehyde levels and protected against catalase exhaustion, but had no significant effect on the NO production. L-arginine had a definite antioxidant effect, which was much weaker than that of VC&VE. In conclusion, antioxidants and a supplement of NO protected the liver tissue against IRI.
机译:缺血再灌注损伤(IRI)被认为是由氧自由基引起的。一氧化氮(NO)也被认为在IRI中起关键作用。本实验旨在评估抗氧化剂和NO补充剂对肝IRI的影响。将雄性Sprague-Dawley大鼠分为五组:假手术组,IRI组和三组维生素C联合维生素E(VC&VE),L-精氨酸和N(G)-硝基-L-精氨酸( NNLA)在IRI之后注射。通过钳夹肝门30分钟然后放松钳制来诱导IRI。为了防止肠系膜血液充血,在门静脉夹闭前四周进行了门体分流术。进行了血液中TNF-α和NO2-,丙二醛,过氧化氢酶活性和NO合酶活性的生化分析。结果如下:IRI提高了丙二醛水平并显着耗尽了过氧化氢酶活性。 VC&VE降低了丙二醛的水平并保护了过氧化氢酶的枯竭,但对NO的产生没有显着影响。 L-精氨酸具有一定的抗氧化作用,远弱于VC&VE。总之,抗氧化剂和一氧化氮的补充保护肝脏组织免受IRI侵害。

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