Protectiveeffectofobeticholicacidonobesity-induced
cardiomyopathy
ChaoLi,ShijunZhang,ZhiboGai,YunlunLi
OBJECTIVESObesityisamajorcontributortomyocardialcellapoptosis,fibrosisandventriclehypertrophy,andassociatedwiththeincreasedriskofhypertrophiccardiomyopathy.Obeticholicacid(OCA),afarnesoidXreceptoragonist,isakeyregulatoroflipidmetabolism,inflammatory,fibrosisandmetabolicpathways.ThisstudywasperformedtoinvestigatetheeffectandmechanismofOCAonobesity-inducedmyocardialinjury.
METHODSC57Bl/6micewerefedwitha45%highfatdiet(HFD)orastandarddiet.Biochemicalparametersandmyocardialpathologicalchangeswereexamined.Energymetabolisminisolatedworkingheartusingradioactivewasalsotestedtorevealthemechanismofmyocardialinjury.Invitro,3Dcellculture,mitochondriadamageandATPproductionofC2C12cellsculturedwithpalmiticacid(PA)intheabsenceorpresenceofOCAweretested.
RESULTSThebodyweightofHFDC57Bl/6micehasincreasedby22.7%
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