三七干预高脂诱导的兔动脉粥样硬化的作用机制

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AbstractObjectiveToobservethemechanismPanaxNotoginsengpowderininterveningwiththeatherosclerosisrabbitsfedwith hyperlipidemiadieMethods：TwentyNewZealhiterabbitsteSprague-Dawleystranwereselectedfedwithigfatdietto establishtheatherosclerosismodelTerabitswereromlyasifiedintotecontrolgroup，themodelgroup，theigdosePanax Notoginsenggroup，thelowdosePanax Notoginsenggroup，with5rabbtsineachgroup.Afteradministrationfor10weeks，erum totalolesterreridndlesilopotenolesteCrettdreftsio wasobservedbyematoxylieosin（HE）stainingeatiolidplaquesareafoedinthearteralvesselsteaortatotetotalarea fthearteriallumentilipidplauearea）wasobseedbyimageanalysismetods.Temberatrixmetalproteiase（P-2） nuclear transcription factor- κB（NF-κB） positive cells in each 0.01mm2 areawas measured by immunohistochemical staining.Results： Compared with the control group，the levels serum TC，TG，LDL-C in the model group increased P<0.05 ）.Comparedwiththe modelgroup，thelevelsserumTC，TG，LDL-Cinthehigh-dosePanaxNotoginsenggroupthelow-dosePanaxNotoginseng group decreased（ P<0.05 ）.Compared with the control group，the expression MMP-2 NF- κB positive cells in the model group increased（ P<0.01 ）.Compared with the model group，the expressions MMP-2 NF- κB positive cells in the high-dose Panax Notoginseng group the low-dose Panax Notoginseng group decreased P<0.01 ）.Compared with the control group，arterial intima area， the ratios lipid plaque areain the model group enlarged（ P<0.05 ）.Comparedwith themodel group，arterial intimaarea， theratio lipidplaqueareainthehigh-dosePanax Notoginsenggroupthelow-dosePanax Notoginsenggroupreduced P<0.05） Conclusin：PanaxNotoginsengpowdermightinhibittheformationatherosclerosisbydecreasingbloodipids，antoxidationnd inhibiting the expression MMP-2 NF-κB ：

Keywordsatroslerosis;anatoie;atrietalopoteae2;ctrascitto;bxptalstuy

动脉粥样硬化（atherosclerosis，AS）是一种常见的，有严重健康风险的疾病，对人类的健康造成了巨大威胁，且AS的发病率逐年升高。（剩余4856字）