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时间:2020-04-02
《针灸疗法对阿尔茨海默病模型大鼠脑啡肽酶和前序列蛋白.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、辽宁中医杂志2014年第41卷第9期·2007·DOI∶10.13192/j.issn.1000-1719.2014.09.091针灸疗法对阿尔茨海默病模型大鼠脑啡肽酶和前序列蛋白酶表达的影响罗琴琴,孙国杰,杜艳军,宋杰,沈峰(湖北中医药大学针灸骨伤学院,湖北武汉430061)摘要:目的:观察针灸百会、肾俞对Aβ1-42所致阿尔茨海默病(AD)模型大鼠脑啡肽酶和前序列蛋白酶的影响。方法:10月龄左右的雄性Wistar大鼠,随机分为正常组、假手术组、模型组、治疗组。采用双侧海马一次性注射凝聚态Aβ1-42制备AD大鼠模型,治疗组选取双侧肾俞穴和百会穴进行针刺和艾灸治疗。采用免疫组织化学法和免疫
2、荧光法检测各组大鼠海马NEP和PreP的变化。结果:模型组大鼠海马NEP和PreP的含量比正常组、假手术组明显降低,其差异具有统计学意义(P<0.01),治疗组大鼠海马NEP和PreP的含量与模型组比较有显著提高(P<0.01)。结论:“益肾调督”针灸疗法可以通过提高大鼠海马NEP和PreP的含量,促进细胞内外β淀粉样蛋白的降解,从而减少其神经毒作用。关键词:针灸疗法;阿尔茨海默病;脑啡肽酶;前序列蛋白酶;益肾调督中图分类号:R285文献标志码:A文章编号:1000-1719(2014)09-2007-03InfluenceofAcupunctureandMoxibustiononNepri
3、lysinandPresequenceProtease'sLevelsinRatswithAlzheimer'sDiseaseLUOQinqin,SUNGuojie,DUYanjun,SONGJie,SHENFeng(Acupuncture&MoxibustionCollege,HubeiUniversityofChineseMedicine,Wuhan430061,Hubei,China)Abstract:Objective:Toinvestigatetheeffectofacupunctureandmoxibustionfortonifyingkidneyandstrengthening
4、marrowonNEPandPreP'slevelsinAβ1-42inducedADrats.Methods:Accordingtotherandomnumbertable,40Wistarratsabout12monthsoldweredividedintofourgroups,10ratsineachone:anormalgroup,asham-operationgroup,amodelgroupandatreatmentgroup.TheAβ1-42incondensedstatewasinjectedintothebilateralhippocampustoprepareADrat
5、model.Intreat-mentgroup,bilateralShenshu(BL23)andBaihui(GV20)wereselectedforthetreatmentofacupunctureandmoxibustion.TheimmunohistochemistrywasadoptedtodetectthechangesofNEPandPrePinhippocampusineachgroup.Results:Comparedwithhippocampusapparently,itindicatedstatisticalsignificantdifference(P<0.01).T
6、hecontentsofhippocampusNEPandPrePintreatmentgroupweresignificantlyhigherthanthoseinmodelgroup(P<0.05).Conclusion:ThetreatmentofacupunctureandmoxibustionfortonifyingkidneyandstrengtheningmarrowcouldhelptodegradetheproteinofAβtoreduceitspoisonbyescala-tingthelevelsofNEPandPrePinthehippocampus.Keyword
7、s:acupunctureandmoxibustion;Alzheimer'sDisease;NEP;PreP;tonifyingkidneyandstrengtheningmarrow目前,虽然阿尔茨海默病(Alzheimer'sDisease,NEP和PreP的影响,为针灸治疗AD的临床应用提供AD)的病因复杂且存在众多争议,但Aβ的异常增多一定的理论基础。及过度累积,已经被确认是导致AD发生发展的关键1
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