猕猴桃果仁油对小鼠非酒精性脂肪性肝病的作用  

Kiwifruit seed oil has a protective effect against nonalcoholic fatty liver disease in mice

作　　者：向志钢[1] 李先辉[1] 刘锋[1] 周卫华[1] 张永康[1] 

机构地区：[1]吉首大学医学院吉首大学医学研究所,湖南省吉首市416000

出　　处：《世界华人消化杂志》2009年第34期3491-3496,共6页World Chinese Journal of Digestology

基　　金：湖南省自然科学基金项目;No.07JJ6029~~

摘　　要：目的:观察猕猴桃果仁油对小鼠非酒精性脂肪性肝病(nonalcoholic fatty liver disease,NAFLD)的保护作用,并初步探讨其作用机制.方法:健康,♂小鼠50只,随机分为:对照组、模型组和果仁油低、中、高剂量组[90、180、270mg/(kg·d)]5组.除对照组用普通饲料喂养外,其余各组均给予高脂饲料喂养.实验6wk后处死全部小鼠,比较各组之间血清和肝脏生化以及肝脏组织病理学特征.结果:与对照组相比,模型组小鼠血清TG、TC、ALT、AST和肝组织MDA显著升高(均P<0.01),肝组织SOD和GSH-Px显著降低(均P<0.01);果仁油中、高剂量组小鼠血清TC、TG、ALT、AST及肝组织MDA显著低于模型组(TC:3.05±0.32mmol/L,2.55±0.43mmol/Lvs4.55±0.23mmol/L;TG:1.62±0.68mmol/L,1.56±0.57mmol/Lvs1.90±0.55mmol/L;ALT:76.91±16.32U/L,64.54±11.32U/Lvs170.34±9.32U/L;AST:128.26±20.15U/L,112.74±21.37U/Lvs158.86±18.45U/L;MDA:5.16±0.97U/mg,5.01±1.14U/mgvs5.88±1.07U/mg,P<0.05或0.01),肝组织SOD和GSH-Px的显著高于对照组(均P<0.05);模型组小鼠肝脏脂肪变性严重,并伴有炎细胞浸润及坏死,而果仁油中、高剂量组小鼠肝脏脂肪变性程度轻,无明显炎细胞浸润及坏死.结论:猕猴桃果仁油对高脂饲料诱导的小鼠非酒精性脂肪性肝病有明显的保护作用.AIM： To investigate whether Kiwifruit seed oil has a protective effect against nonalcoholic fatty liver disease in mice. METHODS： Fifty adult male mice were ran- domly divided into five groups： normal control group, model control group, and three Kiwifruit seed oil treatment groups （low-, medium- and high-dose）. Mice in the normal control group were fed a normal diet, while those in other groups were fed a high-fat diet. Mice in the three Kiwifruit seed oil treatment groups were also given low-, medium- and high-dose Kiwifruit seed oil, respectively. Six weeks later, the body weight, liver index, serum TG, TC, ALT and AST levels, and hepatic TG, TC, MDA, SOD and GSH-Px levels were measured. The histological changes in the liver were evaluated by hematoxylin and eosin （HE） staining and oil red staining. RESULTS： Compared with the normal control group, the liver index, serum TG, TC, ALT and AST levels, and hepatic MDA level markedly increased （all P 〈 0.01）; and hepatic SOD and GSH-Px significantly decreased （both P 〈 0.01） in the model control group. Compared with the model control group, the liver index, serum TG, TC, ALT and AST, and hepatic MDA mark- edly decreased （TC： 3.05 ± 0.32 mmol/L, 2.55 ± 0.43 mmol/L vs 4.55 ± 0.23 mmol/L; TG： 1.62± 0.68 mmol/L, 1.56 ± 0.57 mmol/L vs 1.90 ± 0.55 mmol/L; ALT： 76.91 ± 16.32 U/L, 64.54± 11.32 U/L vs 170.34 ± 9.32 U/L; AST： 128.26± 20.15 U/L, 112.74 ± 21,37 U/L vs 158.86 ± 18.45 U/L; MDA： 5.16 ± 0.97 U/mg, 5.01± 1.14 U/mg vs 5.88 ± 1.07 U/mg; all P 〈 0.05 or 0.01）; and hepatic SOD and GSH-Px significantly increased （both P 〈 0.01） in the medium- and high-dose Kiwifruit seed oil treatment groups. Mice in the model control group showed serious fatty degeneration, inflammatory cell infiltration and necrosis in the liver. However, these pathological changes were milder in the medium- and high-dose Kiwifruit seed oil treatment groups than in the model control group. CONCLUSION： Kiwifruit seed oil has a protective

关 键 词：猕猴桃果仁油 Α-亚麻酸 小鼠 非酒精性脂肪性肝病 

分 类 号：R575[医药卫生—消化系统]