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时间:2018-08-01
《二氮嗪预处理对肝硬化大鼠肝脏的保护作用》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、二氮嗪预处理对肝硬化大鼠肝脏的保护作用作者:史卫海,孙亚伟,徐学忠,戎亚雄,李文美【摘要】目的探讨采用线粒体ATP敏感性钾通道(mitoKATP通道)选择性开放剂二氮嗪(DE)进行预处理能否模拟缺血预处理(IP)对硬化肝脏缺血再灌注损伤的保护作用及其可能的作用机制。方法雄性肝硬化SD大鼠随机分为5组(每组8只)。IP组以肝缺血5min作预处理;DE组以静脉注射DE作为预处理;DE+5-HD组是在DE组基础上再予静注mitoKATP通道选择性阻滞剂5-hydroxydecanoate(5-HD)进行预
2、处理;对照组(C组)以静注等量生理盐水作为预处理;上述4组均在预处理后行肝缺血45min再灌注60min;缺血方式均为70%肝脏热缺血。假手术组(S组)仅行开腹,不作任何其他处理。完成预定实验操作后分别取血用于血清谷丙转氨酶(ALT)与乳酸脱氢酶(LDH)检测,切取肝组织用于测定ATP酶活力、湿重/干重(W/D)的测定及观察显微、超微结构变化。结果C组ALT,LDH,ATP酶及W/D的水平明显高于S组(P<0.01),肝脏的显微及超微结构损伤明显;IP组与DE组的各项肝组织损伤指标均明显好于C
3、组,ATP酶活性低于C组(P<0.05及P<0.01);而DE+5-HD组的肝损伤指标均差于DE组,ATP酶活性高于DE组(P<0.05及P<0.01)。结论13使用DE进行药物预处理能够模拟出IP效应,对肝硬化大鼠肝脏I/R损伤具有保护作用,其作用可能与下调肝组织ATP酶活性,减少ATP大量分解,使肝组织ATP含量升高,改善肝能量代谢,增加能量储备;改善肝组织微循环,减轻肝脏水肿有关。【关键词】缺血预处理;缺血/再灌注;线粒体ATP敏感性钾通道;肝硬化;二氮嗪;大鼠Abst
4、ractObjectiveToexplorewhetherthepretreatmentwithdiazoxide(DE)—aselectiveopenerofmitochondrialATPsensitivepotassium(mitoKATP)channelscanmimictheprotectivefunctionofischemicpreconditioning(IP)onliverischemia/reperfusion(I/R)injuryinratswithcirrhosisandth
5、eprobablemechanism.MethodsMaleSDratswithlivercirrhosiswererandomlydividedintofivegroups(n=8ineachgroup).Pretreatmentwithhepaticischemiafor5minwasregardedasIPgroup;pretreatmentwithDE5mg/kgintravenouslyinjectionwasregardedasDEgroup;pretreatmentwithintrav
6、enousinjectionofaselectivemitoKATPchannelsinhibitor5-hydroxydecanoate(5-HD)baseduponDEgroupwasconsideredasDE+5-HDgroupandpretreatmentwithnormalsalineinequalvolumeasacontrolgroup(Cgroup).Thefourgroupsmentioned-aboveweresubjectedtohepaticischemiafor45min
7、afterpretreatment,then,50minutesreperfusionwasperformed13onthem.Allofratsweresubjectedto70%warmischemia.Theadditionalfifthgroupofratswasundergoneashamoperation(Sgroup),inwhomonlyanesthesiaandlaparotomywereperformedwithoutanyothermeasures.Bloodandlivert
8、issuewereobtainedtodeterminethebiochemistrylevelsandobservepathologicalchanges.ResultsTheactivitiesofALT,LDH,ATPaseandthelevelsofW/DinCgroupwerehigherthanthoseinSgroup(P<0.01).Therewerealsoseverehistologicalandultra-structuraldamagesinC
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