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《《荷叶碱防治小鼠高脂血症作用及其机制》.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、·440·HeraldofMedicineVo1.34No.4April2015荷叶碱防治小鼠高脂血症作用及其机制:}:张丽静,艾耀伟,王政强(三峡大学人民医院、湖北省宜昌市第一人民医院消化内科,宜昌443000)摘要目的研究荷叶碱对饮食诱导的高脂血症小鼠的影响并了解其降脂机制。方法将小鼠根据饲料分为3组:正常对照组(n=1O)、模型对照组(n=10)、干预组(n:lO)。正常对照组采取普通饮食(ANI-76A饲料:12.4%脂肪,68.8%碳水化舍物,18.8%蛋白质);模型对照组采用高脂饮食诱导(高脂饲料:37.1%脂肪,42.4%碳水化合物,20
2、.5%蛋白质);干预组在高脂饲料基础上添加了0.5%荷叶碱。小鼠自由食用,共10周。比较3组小鼠体质量、血脂、脂代谢关键酶、肝脏氧化应激的变化并研究脂质代谢通路。结果高脂饮食成功诱导出高脂血症模型小鼠:肥胖、血脂增高(P<0.05)。干预组与模型对照组比较:小鼠体质量降低[(33.97±3.46)g比(27.624-2.87)g],血脂降低[(2.734-0.26)g比(1.9l+0.21)g],均P<0.05,但不能改善其高甘油三酯血症(P>O.05);肝脂酶活性[(4.154-1.26)U·mL。。比(9.O1±1.34)U·mL]及脂蛋白脂酶活性
3、提高[(8.12_+3.07)u·mL比(13.48_+3.75)U·mL。],且降低了肝脏氧化应激(P4、15)04—0440—05Effects0fNuciferineonMicewithHyperlipidemiaandItsMechanismsZHANGLijing,AIYaowei,WANGZhengqiang(DepartmentofGastroenterology,People’SHospitalofThreeGorgeUniversity,theFirstPeople"sHospitalofYichang,HubeiProvince,Yichang443000,China)ABSTRACT0hiectiveToinvestigatetheef5、f~ctsofnuciferineouhyperlipidemiainmiceandtoclarifythemolecularmechanism.MethodsMiceweredividedintothreegroupsaccordingtothediet:normalcontrolgroup(n=l0),modelcontrolgroup(n=10),andtheinterventiongroup(n=10).Thenormalcontrolgroupwastreatedwithcomulondiet(ANI一76Afeed:12.4%fat,68.6、8%carbohydrate,18.8%protein).Themodelcontro1groupwasinducedwithhighfatdiet(37.1%fat,42.4%carbohydrate.20.5%protein).Theinterventiongroupwassupplementedwith0.5%nuciferinebasedonhighfatdiet.Themicewereallowedfreeaccesstofoodandwaterforatotalof10weeks.Severalindiceswereanalyzedinth7、e3groups,includingthebodyweight,segumlipid,lipidmetabolismkeyenzyme,oxidativestressandmetabolicpathway.ResultsOurresultssuggestedthatthehigh—fatdiet—inducedanimalmodelsdevelopedobesityanddyslipidemia(P<0.05).Thebodyweight[(33.97+3.46)gv5.(27.62±2.87)g]andtheseFumlipid[(2.73±0.268、)g.(1.91±0.21)g]weresignificantlydecreasedinthe
4、15)04—0440—05Effects0fNuciferineonMicewithHyperlipidemiaandItsMechanismsZHANGLijing,AIYaowei,WANGZhengqiang(DepartmentofGastroenterology,People’SHospitalofThreeGorgeUniversity,theFirstPeople"sHospitalofYichang,HubeiProvince,Yichang443000,China)ABSTRACT0hiectiveToinvestigatetheef
5、f~ctsofnuciferineouhyperlipidemiainmiceandtoclarifythemolecularmechanism.MethodsMiceweredividedintothreegroupsaccordingtothediet:normalcontrolgroup(n=l0),modelcontrolgroup(n=10),andtheinterventiongroup(n=10).Thenormalcontrolgroupwastreatedwithcomulondiet(ANI一76Afeed:12.4%fat,68.
6、8%carbohydrate,18.8%protein).Themodelcontro1groupwasinducedwithhighfatdiet(37.1%fat,42.4%carbohydrate.20.5%protein).Theinterventiongroupwassupplementedwith0.5%nuciferinebasedonhighfatdiet.Themicewereallowedfreeaccesstofoodandwaterforatotalof10weeks.Severalindiceswereanalyzedinth
7、e3groups,includingthebodyweight,segumlipid,lipidmetabolismkeyenzyme,oxidativestressandmetabolicpathway.ResultsOurresultssuggestedthatthehigh—fatdiet—inducedanimalmodelsdevelopedobesityanddyslipidemia(P<0.05).Thebodyweight[(33.97+3.46)gv5.(27.62±2.87)g]andtheseFumlipid[(2.73±0.26
8、)g.(1.91±0.21)g]weresignificantlydecreasedinthe
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