资源描述:
《葛根素抗糖尿病大鼠心肌线粒体氧化应激损伤作用研究_顾.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、第28卷第10期中华中医药学刊Vo.l28No.102010年10月CHINESEARCHIVESOFTRADITIONALCHINESEMEDICINEOct.2010葛根素抗糖尿病大鼠心肌线粒体氧化应激损伤作用研究顾掌生,王大力(湖州中心医院,浙江湖州313000)摘要:目的:研究葛根素对链脲佐菌素诱导的I型糖尿病大鼠心功能及心肌线粒体氧化应激的影响。方法:雄性Sprague-Dawley大鼠,随机分成正常对照组,葛根素对照组,糖尿病模型组,低剂量葛根素治疗组,高剂量葛根素治疗组。各组大鼠饲养8周后,测体重、血糖、心功能、左心室重量、心肌胶原含量,分离心肌线粒体检测活性
2、氧自由基(ROS)水平、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果:葛根素治疗组抑制糖尿病大鼠血糖的进一步升高,减少糖尿病引起的体重下降,并且显著减少糖尿病大鼠心室与体重比值,提高左室发展压左心室内压最大上升和下降速率,降低左室舒张末压。葛根素明显减少糖尿病大鼠心肌胶原含量及心肌线粒体ROS水平;高剂量葛根素明显抑制心肌线粒体MDA含量,增加心肌线粒体SOD活性。结论:葛根素治疗糖尿病大鼠8周后,能显著改善糖尿病大鼠心功能,其机制可能与抑制血糖升高,减轻心肌线粒体氧化应激损伤有关。关键词:葛根素;糖尿病;心功能损伤;线粒体氧化应激中图分类号:R285.5文献标
3、识码:A文章编号:1673-7717(2010)10-2197-04PuerarinReducesMitochondrialOxidativeStressInjuryinDiabeticRatHeartsGUZhang-sheng,WANGDa-li(HuzhouCenterHospita,lHuzhou313000,Zhejiang,China)Abstrac:tAim:Toinvestigatetheeffectsofpuerarinoncardiacfunctionsandmitochondrialoxidativestressinstrep-tozotocin(ST
4、Z)-induceddiabeticrats.Methods:MaleSprague-Dawleyratswererandomlydividedintoanormalcon-trolgroup,apuerarincontrolgroup,adiabeticgroup,anddiabeticgroupsadministeredwithalowdoseorahighdoseofpuerarinfor8weeks.Thebodyweight,bloodglucose,cardiacfunctions,leftventricularweight,andmyocardialcolla
5、genlevelwereassayed.Thecardiacmitochondrialreactiveoxygenspecies(ROS)leve,lmalondialdehyde(MDA)leve,landsuperoxidedismutase(SOD)activityweremeasured.Results:Treatmentwithpuerarininhibitedtheincreaseofbloodglucoseandreducedthelosingofbodyweightindiabeticrats.Puerarinmarkedlyreducedtheratioo
6、fventricularweightandbodyweight,increasedtheleftventriculardeveloppressureanddP/dtmax,anddecreasedtheleftventricularendd-iastolicpressureindiabeticrats.ThemyocardialcollagenandthelevelofcardiacmitochondrialROSindiabeticratswereallmarkedlyreducedbypuerarin.Furthermore,highdoseofpuerarinsign
7、ificantlydecreasedthemitochondrialMDAlev-elandincreasedSODactivityindiabeticrathearts.Conclusion:Treatmentwithpuerarinfor8weeksmarkedlyimprovesthecardiacfunction,whichmayberelatedtoinhibitingtheincreaseofbloodglucoseandreducingmitochondrialoxidativestressinjur