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有机硒保护肝损伤组织脂质过氧化反应及其机制研究
引用本文:蒋英子,陈龙,潘道东,曹萌,朱善良,周娟. 有机硒保护肝损伤组织脂质过氧化反应及其机制研究[J]. 营养学报, 2005, 27(2): 105-109
作者姓名:蒋英子  陈龙  潘道东  曹萌  朱善良  周娟
作者单位:1. 南京师范大学生命科学学院
2. 南京师范大学食品科学系,南京,210097
基金项目:江苏省资源生物技术重点实验室开放基金(No.KJS00033)
摘    要:目的:研究乳酸菌源有机硒保护肝损伤组织脂质过氧化反应及其机制。方法:选择93只健康、雌雄对半成年小鼠,分两个系列进行实验。系列I:36只小鼠随机分成对照组(C组),CCl4组、CCl4-有机硒保护组(CCl4-Se组),通过腹腔注射CCl4诱发肝损伤后,分别在第2、4w观察肝组织匀浆中的GSH-Px、CAT、SOD和MDA的变化。系列II:48只小鼠随机分为C组、CCl4组、CCl4-低剂量有机硒保护组(CCl4-LSe组)、CCl4-高剂量有机硒保护组(CCl4-HSe组),饲养7d后通过腹腔注射CCl4诱发肝损伤,再分别在D4、D8采用激光共聚焦显微镜技术,观察各组动物肝细胞[Ca2+]i的变化。结果:在整个实验期内,肝组织匀浆CCl4组MDA含量明显高于C组和CCl4-Se组,CCl4-Se组与C组接近;CCl4-Se组GSH-Px和CAT活性较CCl4组高,但低于C组;SOD活性三组间虽无显著差异,但C组和CCl4-Se组均较CCl4组高;实验D4,CCl4组肝细胞[Ca2+]i浓度的平均荧光像素是C组的2.8倍,到了D8是C组的5.5倍,而CCl4-Se组均明显低于CCl4组,与C组较为接近。结论:乳酸菌源有机硒可能通过抗损伤保护肝细胞[Ca2+]i稳态而减轻由CCl4诱发的肝损伤过程。

关 键 词:乳酸菌  有机硒  肝损伤  脂质过氧化  钙离子
文章编号:0512-7955(2005)02-0105-05
修稿时间:2004-05-14

STUDY ON THE PROTECTIVE EFFECT OF ORGANOSELENIUM FROM SE-ENRLED LACTOBACILLUS ON CHEMICAL LIVER INJURY AND ITS MECHANISM
JIANG Ying-zi,CHEN Long,PAN Dao-dong,CAO Meng,ZHU Shan-liang,ZHOU Juan. STUDY ON THE PROTECTIVE EFFECT OF ORGANOSELENIUM FROM SE-ENRLED LACTOBACILLUS ON CHEMICAL LIVER INJURY AND ITS MECHANISM[J]. Acta Nutrimenta Sinica, 2005, 27(2): 105-109
Authors:JIANG Ying-zi  CHEN Long  PAN Dao-dong  CAO Meng  ZHU Shan-liang  ZHOU Juan
Affiliation:JIANG Ying-zi,CHEN Long1,PAN Dao-dong1,CAO Meng1,ZHU Shan-liang,ZHOU Juan
Abstract:Objective: To study the protective effect in CCl4-induced liver injury by organoselenium from Se-enriched lactobacillus. Methods: (1) In the first series, forty-five animals were randomly divided into control (C) group, CCl4 group, CCl4 plus organoselenium group (CCl4-Se group). The liver injury was induced by abdominal injection of CCl4 every other day for 4 w. Changes of GSH-Px, CAT and SOD activities as well as MDA content in liver were estimated in the 2nd and 4th week after CCl4 injection respectively. (2) In the second series, forty-eight mice were randomly divided into C group, CCl4 group, CCl4 plus low dose organoselenium group (CCl4-LSe group) and CCl4 plus high dose organoselenium group (CCl4-HSe group). Changes of hepatocyte [Ca2 ]i in animals in every group were investigated by means of confocal laser microscope on the 4th and 8th day after CCl4 injection respectively. Results: During the entire experimental period, liver MDA of CCl4 group was markedly superior to that of C and CCl4-Se groups, and the level of latter two groups was very close. The GSH-Px and CAT activities were higher in CCl4-Se group than in CCl4 group,but lower than that of C group. There were higher SOD activities in C and CCl4-Se groups compared to that in CCl4 group though without obvious difference. Average fluorescence pixels of hepatocyte [Ca2 ]i in CCl4 group was 2.8 and 5.5 times higher than that of group C in the 4th and 8th day respectively,while those in CCl4-Se groups were significantly lower than those of CCl4 group, and close to C group. Conclusions: Organoselenium from Se-enriched lactobacillus, can protect hepatocyte [Ca2 ]i homeostasis by reducing lipid peroxidation after CCl4 exposure.
Keywords:Lactobacillus  organoselenium  liver injury  lipid peroxidation  calcium ions
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