二甲基硫脲对心肌细胞抗过氧化氢损伤的实验研究  

Anexperimentalstudyoftheeffectofdimethylthioureaonmyocardialcelinjuryinducedbyhydro┐genperoxide

作　　者：陈广文[1] 刘世坤[1] 罗涵[1] 

机构地区：[1]湖南医科大学病理生理教研室

出　　处：《中华心血管病杂志》1996年第6期452-454,共3页Chinese Journal of Cardiology

摘　　要：为探讨二甲基硫脲（ＤＭＴＵ）保护心肌细胞抗过氧化氢（Ｈ２Ｏ２）损伤。３２瓶培养乳鼠心肌细胞随机分４组，每组８瓶：（１）对照组；（２）Ｈ２Ｏ２（５ｍｍｏｌ）组；（３）ＤＭＴＵ（２０ｍｍｏｌ）组；（４）Ｈ２Ｏ２（５ｍｍｏｌ）＋ＤＭＴＵ（２０ｍｍｏｌ）组。在３７℃、５％ＣＯ２的ＭＥＭ培养４小时。结果发现：（１）与对照组比，Ｈ２Ｏ２组乳酸脱氢酶（ＬＤＨ，Ｕ／１００ｍｌ）释放多（２８２．３８±４７．２８比７７．２５±１８．２５，Ｐ＜０．０１）、ＴＢＡ反应物（ＴＢＡＲＳ，ｎｍｏｌ／ｍｇＰｒ．）产生多（２．２５±０．５３比０．７９±０．３６，Ｐ＜０．０１）；（２）与Ｈ２Ｏ２组比，Ｈ２Ｏ２＋ＤＭ－ＴＵ组ＬＤＨ释放少（９９．２５±４１．８８比２８２．３８±４７．２８，Ｐ＜０．０１）；ＴＢＡＲＳ产生少（０．５９±０．１８比２．２５±０．５３，Ｐ＜０．０１）；此外，我们还发现ＤＭＴＵ组超氧化物歧化酶（ＳＯＤ，μｇ／ｍｇＰｒ．）比对照组高（８．４９±３．６５比１．９２±１．４０，Ｐ＜０．０１）。ＤＭＴＵ能保护心肌细胞抗Ｈ２Ｏ２损伤，机制与灭活羟自由基（·ＯＨ）。Weinvestigatedwhetherdimethylthiourea(DMTU)mayprotectculturedmyocardialcelfrominjuryinducedbyhydrogenperoxide(H2O2).32botlesofculturedratneonatalcardiomy-ocytesweredividedinto4groupsrandomly(8botlesineach):controlgroup;H2O2(5mmol)group;DMTU(20mmol)group;andH2O2(5mmol)plusDMTU(20mmol)group.Thecardiomy-ocytesamong4groupswereculturedwithMEMcelculturedsolutionat37℃inthepresenceof5%CO2for4hours.Incomparingwiththecontrolgroup,thereleaseoflacticdehydrogenase(LDH)andtheproductionofthiobarbituricacidreactionsubstance(TBARS)intheH2O2groupincreasedsignificantly(LDH,282.38±47.28vs77.25±18.25,P<0.01;TBARS,2.25±0.53vs0.79±0.36,P<0.01).IncomparingwiththeH2O2group,thereleaseofLDHandproductionofTBARSintheH2O2plusDMTUgroupdecreasedsignificantly(LDH,99.25±41.88vs282.38±47.28,P<0.01;TBARS,0.59±0.18vs2.25±0.53,P<0.01).Inaddition,theactivityofsuperoxidedismu-tase(SOD)intheDMTUgroupwashigherthanthatinthecontrolgroup(8.49±3.65vs1.92±1.40,P<0.01).ThesedatasuggestthatDMTUcouldprotectcardiomyocytesfromtheH2O2in-ducedinjurybecauseofitsabilitytoincreaseSODactivityincardiomyocytesexceptforitsdirectinac-tivityofhydroxylfreeradical(·OH).

关 键 词：二甲基硫脲 心肌缺血 再灌注损伤 过氧化氢 

分 类 号：R541.405[医药卫生—心血管疾病]