维生素E和硒对CCl_4大鼠急性肝损伤和抗氧化功能的影响

Influences of Vitamin E and Selenium on Acute Liver Injury Induced by CC1_4 in Rats and Their Antioxidative Function

背景:氧应激在急性肝损伤的发生过程中具有重要作用,因此提高机体的抗氧化功能对防治急性肝损伤具有重要意义。目的:探讨维生素E(Vit E)和硒对CCl4大鼠急性肝损伤和抗氧化功能的影响。方法:48只健康雄性SD大鼠随机分为6组,每组8只。干预组第1周和第2周以及造模组第1周和第2周采用腹腔注射50% CCl4和橄榄油混合制剂的方式建立大鼠急性肝损伤模型,干预组在饲料中添加Vit E(250 mg/kg饲料)和硒(O.2 mg/kg饲料)进行营养干预,造模组喂饲标准饲料;对照组第1周和第2周腹腔注射生理盐水,喂饲标准饲料。第1周和第2周组大鼠分别于处理1周和2周后处死,分别检测各项肝损伤指标和抗氧化指标,并观察其含量变化。结果:对于急性肝损伤大鼠,补充适量的Vit E和硒能降低血清丙二醛(MDA)水平,干预组的血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)升高幅度明显较造模组小,肝组织羟脯氨酸含量亦相对低于造模组。造模组的肝组织和血清硒水平在第2周明显升高,而Vit E水平显著降低,并伴随着超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPX)活性的显著升高,而干预组的各项指标基本维持不变。结论:CCl4致大鼠急性肝损伤时,机体对抗氧化营养素的需求明显上升,补充Vit E和硒后,机体拮抗氧应激所致急性肝损伤的能力增强。

Background: Oxidative stress plays a key role in the development of acute liver injury, so the elevation of antioxidative ability has an important effect on anti-acute liver injury. Aims: To investigate the effect of vitamin E (Vit E) and selenium on acute liver injury in the CCl4-induced rats and their antioxidative function. Methods: Forty-eight normal male SD rats were randomly divided into six groups (8 rats/group): interventional group (the first week and the second week), model group (the first week and the second week), and control group (the first week and the second week). The interventional and model groups were given intraperitoneal CC14 (diluted with an equal volume of olive oil). The control group received normal saline injection. The rats in the interventional group were fed chow supplement with Vit E (250 mg/kg diet) and selenium (0.2 mg/kg diet), and the other groups were given standard chow. The rats in the first week group were sacrificed after one-week injection, the other groups were put to death after two weeks injection. The markers of acute liver injury and antioxidative function were detected and their changes were observed. Results: The serum level of malondialde-hyde (MDA) was lower; the increase in serum alanine aminotransferase (ALT) and aspartate amino-transferase (AST) was less markedly, and the hydroxyproline level in liver tissue in the interventional group was lower than those in the model group. In the second week, the selenium level of liver tissue and of serum in the model group was increased, while the Vit E level was significantly reduced with elevation of superoxide dismutase (SOD) and glutathione peroxidase (GPX). However, the status of the above indicators in the interventional group maintained unchanged. Conclusions: The demand of antioxidative nutrients can be notably elevated during acute liver injury induced by CC14 in rats, and the ability to resist acute damage of the liver caused by oxidative stress can be enhanced by supplementation with Vit E and selenium.