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1、第42卷第7期山东大学学报(理学版)2007年7月Vol.42No.7JOURNALOFSHANDONGUNNERSITY厄.2007文章编号:1671-9352(2007)07-0001-04壳寡糖及其衍生物对CC14诱导的小鼠肝损伤的保护作用金黎明‘,杨艳2*,刘万顺2,韩宝芹“,田文杰‘,范圣第’(1.大连民族学院生命科学学院,辽宁大连116600;2中国海洋大学海洋生命学院,山东青岛266003)摘要:研究壳寡糖(COS)I氛基葡萄糖(G1cNH2)和N-乙酞氛基葡萄糖(G1cNAc)对CCI,诱导的雄性昆明种小鼠肝毒性的
2、保护作用,并探讨其可能机制.小鼠腹腔注射CCI,(20mg/吨体重)24h后,血清天门冬氨酸转氨酶(AST)和丙氨酸转氛酶(ALT)活性明显提高,引起肝脏脂质过氧化反应,筑基含量降低,总杭氧化能力(T-AOC)减弱,诱发基因毒性.提前连续12天分别灌胃给予COS,G1cNHz和G1cNAc(1.5岁掩体重)能够显著诱导金属硫蛋白(MT)的表达,体内的抗氧化防御系统随之增强以抵抗CCI,诱导的氧化损伤.血清ASI,和ALT活性明显降低,肝脏丙二醛(MDA)生成被抑制,筑基含量,T-AOC明显恢复.但是,从DNA电泳结果反应出的基因毒
3、性并未减轻实验结果证明,提前给予COS,G1cN践和G1cNAc对C以诱导的小鼠肝损伤能够起到有效的保护作用,其中,G1cNH2的作用效果最显著.关键词:Ca";壳寡糖;抗氧化;肝保护中图分类号:8931.71文献标识码:AProtectiveeffectsofchitosanoligosaccharideanditsderivativesoncarbontetrachloride一inducedliverdamageinmiceJINIa-mingl,YANGYang‘,LIUWan-shunt,HANBao-gin2,MNWe
4、n-j1e1andFANSheng-di1(1.CollegeofLifeScience,DalianNationalitiesUniv.,Dalian116600,Liaoning,China;2.CollegeofMarineLifeScience,OceanUniversityofChina,Qingdao266003,Shandong,China)Abstract:Theprotectiveeffectsofchitosanoligosaccharide(COS),D-glucosamine(G1cNH2)andN-ace
5、tyl-D-glucosamine(Gl-cNAc)oncarbontetrachloride(CCI,)inducedhepatotoxicityinmaleICRmicewereinvestigatedandthepossiblemechanismsinvolvedwerediscussed.CCI4(20mg/kgbodyweight)administrationinducesmarkedincreaseinserumASTandALTactivities,primesliverlipidperoxidation,deple
6、tessulfhydrylcontent,impairstotalantioxidantcapabilities(T-AOC)andinducesgenotoxic-ity24hafteradministration.PretreatmentwithCOS,G1cNH2,andGlcNAc(1.5g/kgbodyweight)for12consecutivedayspriortoCCI,challengesignificantlyinducesmetallothionein(MT)expression.Thus,theantiox
7、idantdefensivesysteminthebodyisstrengthenedtocounteracttheoxidativedamageinduced场theCCI,administration.SerumASTandALTactivities,effectivelydecreased.Hepaticmalondialdehyde(MDA)formationisinhibited,andsulfhydrylcontentsandT-AOCaremarkedlyrestored.Genotoxicityasreflecte
8、d场DNAfragmentation,however,itisnotmitigated场pretreatmentwithCOS,G1cNH2,andG1cNAc.TheresultssuggestthatpretreatmentwithCOS,G1