摘要
本文主要研究了油茶对高脂饮食引起的大鼠肝损伤的保护作用。试验中将大鼠分为空白对照组、高脂模型组、油茶低、中和高剂量组,每组10只。经造模期15 d和给样期32 d后,腹主动脉采血,取肝脏。测定大鼠肝脏重量,观察肝脏组织病理;分别测定血清中ALT和AST活力,血清和肝匀浆中SOD、GSH-Px活力和MDA水平。结果表明,与高脂模型组相比,油茶组肝脏系数显著降低(p<0.05);血清中ALT和AST活力显著降低(p<0.05);血清和肝脏中SOD和GSH-Px活力显著升高,MDA含量显著降低(p<0.05);肝脏组织病理显示,油茶组能够减轻肝细胞脂肪变性。由结果可知:油茶能够缓解高脂饮食大鼠肝脏肥大,增强机体抗脂质过氧化能力,缓解肝脏脂肪变性,对肝脏损伤起到有效的保护作用,其中油茶高剂量组作用最明显。
This study aimed to investigate whether oil tea（OT） could protect against hepatic damage induced by a high-fat diet（HFD） in rats. In this experiment, 50 rats were randomly divided into five groups, including the untreated control group, HFD control group, and low, medium, and high-dose OT groups, with 10 rats in each group. After the HFD-modeling period of 15 days and OT administration of 32 d, blood samples were collected from the abdominal aorta, and livers were harvested simultaneously. Liver weights were recorded and histopathologic slides were prepared and observed. The activities of alanine transaminase（ALT） and aspartate transaminase（AST） in serum, and the activities of superoxide dismutase（SOD） and glutathione peroxidase（GSH-Px）, and malondialdehyde（MDA） levels in the serum and liver were measured. The results showed that compared with the HFD control group, the liver index of OT groups was significantly decreased（p 0.05）, ALT and AST activities in serum were significantly reduced（p0.05）, SOD and GSH-Px activities in the serum and liver were significantly increased, and the level of MDA was significantly lowered（p0.05）. Hepatic histopathology indicated that OT could relieve hepatic steatosis in rats. These results demonstrate that OT can alleviate hepatic hypertrophy, enhance the body＇s anti-lipid peroxidation ability, relieve fatty degeneration of liver, and exert a protective effect on hepatic damage in HFD rats. In addition, the most effective group was the high-dose OT group.
出处
《现代食品科技》
EI
CAS
北大核心
2017年第1期14-19,共6页
Modern Food Science and Technology
基金
广西高校特色农产品精深加工与安全控制重点实验室资助
广西"食品生物技术"岗位八桂学者团队资助
关键词
油茶
高脂饮食
肝功能
脂质过氧化
oil tea
high-fat diet
hepatic function
lipid peroxidation
