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1、血脂康预处理对心肌缺血再灌注大鼠炎症因子影响【摘要】目的观察血脂康预处理对急性心肌缺血再灌注损伤大鼠炎症因子的影响，探讨其可能的作用机制。方法健康SD大鼠32只，随机分为空白组、假手术组、缺血再灌注组和血脂康预处理组，各8只。血脂康预处理组每天灌胃给予血脂康胶囊0.09g/kg,其余各组给予等量生理盐水，连续7d。缺血再灌注组和血脂康预处理组大鼠均开胸并结扎冠状动脉前降支30min,然后再通60min;假手术组只开胸不结扎冠状动脉，空白组不做任何处理。采集大鼠腹主动脉血,分离血清,检测白细胞介素(IL)1B、IL4、IL&肿瘤坏死因子(TNFa)、肌酸激酶同工酶
2、(CKME)、肌钙蛋白I(cTNI)含量，并处死动物取出心脏，计算心肌梗死面积。结果缺血再灌注组IL10、IL4、IL8、TNFa、CKME和cTNI血清含量均明显高于空白组和假手术组(F=48.72~351.0乙q=0・25〜4外均低于缺41.65,P<0.01);W血脂康预处理组上述指标除IL血再灌注损伤组(q=0・35〜32・65,P<0・05),且血脂康预处理组大鼠心肌梗死面积小于缺血再灌注损伤组(F=231.26,q=17.21,P<0.05)o结论血脂康能抑制促炎因子IL邛、IL8、TNFa的生成，并增加抗炎因子IL4生成，减轻心肌
3、缺血再灌注损伤，对缺血再灌注损伤具有明显的保护作用。【关键词】心肌；再灌注损伤；炎症；白细胞介素类；大鼠,SpragueDawley[ABSTRACT]ObjectiveToobservetheeffectsofXuezhikangcapsulesoninflammatoryfactorofmyocardialischemiareperfusioninjury(MIRI)inratsandexploreitspossiblemechanismofaction.MethodsThirtytwoSDratswereevenlyrandomizedtofourgrou
4、ps:blankgroup,shamoperationgroup,MIRIgroupandXuezhikangpretreatmentgroup・TheratsinXuezhikanggroupweretreatedwithXuezhikang(0.09g-kg-1•d-1,gastricgavage)andothergroupsweretreatedwiththesameamountofsaline,for7days・ThoseinMIRIandXuezhikangpretreatmentgroupsunderwentathoracotomyandthelef
5、tanteriordescendingbranchofcoronaryarterywasligatedfor30minutesandthenrecanalizedfor60minutes;thoseinshamoperationgroupreceivedonlythoracotomywithnoligationofcoronaryartery;noanymanagementwasdoneforthoseintheblankgroup.Bloodsampleswereextractedfromtheabdominalaorta,andtheserumseparat
6、ed.Theinterleukin1(3(ILip),IL4,IL8,tumornecrosisfactoralpha(TNFa),creatinekinaseMB(CKMB),andtroponinlweredetected・Theareaofmyocardialinfarction(MI)wascalculated・ResultsInMIRIgroup,theserumlevelsofILlp,IL4,IL8,TNFa,CKMB,andcTNIweresignificantlyhigherthanthoseofnormalgroupandshamoperat
7、iongroup(F=48.72-351.07,q=0.25-41.65,P<0.01),whiletheaboveparametersinthepretreatmentgroupwerelowerthanthoseofMIRIgroup,exceptIL4(F=48.72-351,q=0.35-32.65,P<0.05).TheareaofMIinXuezhikangpretreatmentgroupwassmallerthanthoseintheMIRI(F=231.26,q=17.21,P<0.05).ConclusionXuezhika
8、ngcaninhibit
