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Effects of methyl protodioscin on i and ATPase activity incardiomyocytes and analysis of mechanisms

甲基原薯蓣皂苷对心肌细胞内钙及ATP酶功能的影响及其机制



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Vol.35,Issue 1
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·18·
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January,2010
A.
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·28·
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Vol.35,Issue 1
January,2010
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—˜™š

[1] 
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HPLC
/NëOrÂýä$LMNïxƒx!
[J]
$%$,23
,2006,31(7):605
[2] 
,G0

,&

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ä

LMNïx•=

ƒ¾Wù
[J]
$%$,23
,2002,27(10):777
[3] HuK,DongA,YaoX,etalAntineoplasticagents;IThree
spirostanolglycosidesfromrhizomesofDioscoreacoletivarhypo
glauca[J]PlantaMed,1996,62(6):573
[4] 
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[J].
$%;,2006,11(6):1168
[5] QiuYing,LiYongyu,LiShuguang,etalEfectofQingyitangon
activityofintracelularCa2+Mg2+ATPaseinratswithacutepan
creatitis[J]WorldJGastroenterol,200410(1):100
[6] 
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LMNï%wÆOžOæÀDE#Ë
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[J]
–,ÓDE
,1994,13
(2):77
Efectsofmethylprotodioscinon[Ca2+]iandATPaseactivityin
cardiomyocytesandanalysisofmechanisms
NINGZong1,LIYikui2,ZHANGRongli3
(1FirstAfiliatedHospitalofGuangXiMedicalUniversity,Nanning530021,China;
2XiyuanHospital,ChinaAcademyofTraditionalChineseMedicine,Beijing100091,China;
3InstituteofMolecularMedicine,PekingUniversity,Beijing100871,China)
[Abstract] Objective:Tostudytheefectsofmethylprotodioscinonthe[Ca2+]iandtheATPaseactivityincardiomyocytes,
aswelastheirmechanisms.Method:Thecardiomyocyteswererandomlydividedintothreegroups,thecontrolgrouptreatedwithno
serumalDMEM,theMPDgrouptreatedwithMPDandthedilthiazemgrouptreatedwithdilthiazem.Fluorospectrophotometerwasused
todeterminedthelevelofmyocardialcelintracelularCa2+[Ca2+]i.IntheexperimentofATPaseactivityoncelularmembrane,the
cardiomyocyteswererandomlydividedintotwogroups,thecontrolgrouptreatedwithnoserumalDMEM,theMPDgrouptreatedwith
MPD.TheactivityofNa+K+ATPase,Ca2+Mg2+ATPaseandMg2+ATPATPaseweredetermined.Thequantitativeanalysisof
SERCA2amRNAexpressionwasstudiedbyRTPCRthatthegroupsandtreatmentsincardiomyocytessameastheexperimentforAT
Paseactivityassay.Result:Underthequiescentcondition,comparedtothecontrolgroup,thelevelof[Ca2+]iincardiomyocytesof
theMPDgroupanddilthiazemgroupwasnodiferent.Aftertreatmentwith40mmol· L-1KCl,[Ca2+]iwassignificantlylowerinthe
MPDgroupandthedilthiazemgroup,andtheintensityofpeakvalueintimecourseof60s,thedilthiazemgroupandtheMPDgroup
alsowerelowerthanthecontrolgroup(P<0.001).Ca2+Mg2+ATPaseandNa+K+ATPaseinculturedratwereincreasedafter
treatedwithMPDcomparedtotreatmentwithnoserumalDMEM(P<0.05,P<0.01),butMg2+ATPaseinthesegroupshadnodif
ferent.TheexpressionofSERCA2amRNAbetweentheMPDgroupandthecontrolgroupwasnodiferent.MPDcouldnotupregulated
ordownregulatedSERCA2ainendocytoplasmicreticulum.Conclusion:Methylprotodioscincouldblockthevoltdependentformcalci
umchannelincelularmembrane,andupregulatethefunctionofsodiumpumpandcalciumpump,sothatitcouldremainlowcalcium
intheinternalenvironmentincardiomyocytes.
[Keywords] methylprotodioscin;cardiomyocyte;[Ca2+]i;ATPaseactivity;SERCA2a
doi:10.4268/cjcmm20100117

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