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时间:2019-05-13
《不同药物对急性胰腺炎小鼠树突细胞的干预作用研究》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、万方数据中国危重病急救医学2010年4月第22卷第4期CllinCritCareMed,April2010,Vol02,N9.4不同药物对急性胰腺炎小鼠树突细胞的干预作用研究王海曼张淑文【摘要】目的探讨急性胰腺炎(AP)免疫学发病机制,同时观察善宁、厚朴酚的干预作用。方法90只BALB/c小鼠按随机数字表法均分为正常对照组、模型组、善宁组、厚朴酚组、联合治疗组,每组18只。采用连续7次腹腔注射雨蛙素的方法制备小鼠AP模型,每次间隔1h;善宁于每次注射雨蛙素前30min皮下注射;厚朴酚于制模完成后即刻尾静脉
2、注射。于制模后9、12、24h摘除小鼠眼球取血,检测外周血淀粉酶、白细胞介素一10(IL一10)、■干扰素(IFN一7)水平;处死动物取脾脏和胰腺,用流式细胞仪检测髓系树突细胞(MDSs)与淋巴系树突细胞(LDCs)数量及其比值;进行胰腺组织病理评分。结果与正常对照组[血淀粉酶(1.12士o.05)kU/L,胰腺病理评分(0.09士o.10)分]比较,模型组血淀粉酶[(26.11士1.96)kU/L]及胰腺病理评分[(5.32士o.19)分]均显著升高(均P3、下降趋势,以制模后9h最显著(o.421士o.049比1.712±o.372,尸4、9、12、24h显著高于善宁组(9h:4.694士0.527比O.819土O.182,12h:2.566士0.463比1.421±O.163,24h:2.343士O.359比1.421士o.113,P<0.05或P5、过调节树突细胞不同亚型的分化,促进Tho向Th2分化,增强抗炎作用,减轻局部及全身炎症反应;善宁未显示出此作用。【关键词】胰腺炎,急性}雨蛙肽,树突细胞;细胞因子}善宁;厚朴酚TheiⅡterventioneffectsofdiffeI.entdn2sondeⅡdriticcellsinacutepancreatitisinmouseH,月』叭;ji台i一竹m,zHANGsh删腿.Dep叭撇mofl托如c谯ot‘sDiseases,B嘶洒gFrie饨dsh争Hos苣'nn王A像ti口tedtotkC口争主6、talMedicazU'l主口ersit,,Beijing100050,Chi,l口C锄spD,ldi,zg口“髓D,.:Z.日A』、rG.S^甜一铂煳,E,,;盘iZ:zjza40jjD囝矗,14.∞,雄【Abstract】0bjectiveTostudytheimmunologicmechanisminpathogenesisoftheacutepancreatitis(AP)andtheinterventioneffectsofsandostatinandmagnol01.MethoibNinety7、BALB/cmiceweredividedintonegativecontrolgroup,caerulein—inducedmodelgroup,sandostatin—treatmentgroup,magnolol—treatmentgroup,combinedsandostatin—andmagnolol—treatmentgroupbymeansofrandomnumbertable,with18miceineachgroup.APmodelwasreproducedbysevenintraper8、itorlealinjectionsofcaeruleinatanintervalof1hour.Every30minutesbeforethecaeruleinchallenge,sandostatinwasinjectedsub—cutaneously.1订agnololwasinjectedintravenouslyimmediatelyaftertheAPmodelwasreproduced.Thenat9,12,24
3、下降趋势,以制模后9h最显著(o.421士o.049比1.712±o.372,尸4、9、12、24h显著高于善宁组(9h:4.694士0.527比O.819土O.182,12h:2.566士0.463比1.421±O.163,24h:2.343士O.359比1.421士o.113,P<0.05或P5、过调节树突细胞不同亚型的分化,促进Tho向Th2分化,增强抗炎作用,减轻局部及全身炎症反应;善宁未显示出此作用。【关键词】胰腺炎,急性}雨蛙肽,树突细胞;细胞因子}善宁;厚朴酚TheiⅡterventioneffectsofdiffeI.entdn2sondeⅡdriticcellsinacutepancreatitisinmouseH,月』叭;ji台i一竹m,zHANGsh删腿.Dep叭撇mofl托如c谯ot‘sDiseases,B嘶洒gFrie饨dsh争Hos苣'nn王A像ti口tedtotkC口争主6、talMedicazU'l主口ersit,,Beijing100050,Chi,l口C锄spD,ldi,zg口“髓D,.:Z.日A』、rG.S^甜一铂煳,E,,;盘iZ:zjza40jjD囝矗,14.∞,雄【Abstract】0bjectiveTostudytheimmunologicmechanisminpathogenesisoftheacutepancreatitis(AP)andtheinterventioneffectsofsandostatinandmagnol01.MethoibNinety7、BALB/cmiceweredividedintonegativecontrolgroup,caerulein—inducedmodelgroup,sandostatin—treatmentgroup,magnolol—treatmentgroup,combinedsandostatin—andmagnolol—treatmentgroupbymeansofrandomnumbertable,with18miceineachgroup.APmodelwasreproducedbysevenintraper8、itorlealinjectionsofcaeruleinatanintervalof1hour.Every30minutesbeforethecaeruleinchallenge,sandostatinwasinjectedsub—cutaneously.1订agnololwasinjectedintravenouslyimmediatelyaftertheAPmodelwasreproduced.Thenat9,12,24
4、9、12、24h显著高于善宁组(9h:4.694士0.527比O.819土O.182,12h:2.566士0.463比1.421±O.163,24h:2.343士O.359比1.421士o.113,P<0.05或P5、过调节树突细胞不同亚型的分化,促进Tho向Th2分化,增强抗炎作用,减轻局部及全身炎症反应;善宁未显示出此作用。【关键词】胰腺炎,急性}雨蛙肽,树突细胞;细胞因子}善宁;厚朴酚TheiⅡterventioneffectsofdiffeI.entdn2sondeⅡdriticcellsinacutepancreatitisinmouseH,月』叭;ji台i一竹m,zHANGsh删腿.Dep叭撇mofl托如c谯ot‘sDiseases,B嘶洒gFrie饨dsh争Hos苣'nn王A像ti口tedtotkC口争主6、talMedicazU'l主口ersit,,Beijing100050,Chi,l口C锄spD,ldi,zg口“髓D,.:Z.日A』、rG.S^甜一铂煳,E,,;盘iZ:zjza40jjD囝矗,14.∞,雄【Abstract】0bjectiveTostudytheimmunologicmechanisminpathogenesisoftheacutepancreatitis(AP)andtheinterventioneffectsofsandostatinandmagnol01.MethoibNinety7、BALB/cmiceweredividedintonegativecontrolgroup,caerulein—inducedmodelgroup,sandostatin—treatmentgroup,magnolol—treatmentgroup,combinedsandostatin—andmagnolol—treatmentgroupbymeansofrandomnumbertable,with18miceineachgroup.APmodelwasreproducedbysevenintraper8、itorlealinjectionsofcaeruleinatanintervalof1hour.Every30minutesbeforethecaeruleinchallenge,sandostatinwasinjectedsub—cutaneously.1订agnololwasinjectedintravenouslyimmediatelyaftertheAPmodelwasreproduced.Thenat9,12,24
5、过调节树突细胞不同亚型的分化,促进Tho向Th2分化,增强抗炎作用,减轻局部及全身炎症反应;善宁未显示出此作用。【关键词】胰腺炎,急性}雨蛙肽,树突细胞;细胞因子}善宁;厚朴酚TheiⅡterventioneffectsofdiffeI.entdn2sondeⅡdriticcellsinacutepancreatitisinmouseH,月』叭;ji台i一竹m,zHANGsh删腿.Dep叭撇mofl托如c谯ot‘sDiseases,B嘶洒gFrie饨dsh争Hos苣'nn王A像ti口tedtotkC口争主
6、talMedicazU'l主口ersit,,Beijing100050,Chi,l口C锄spD,ldi,zg口“髓D,.:Z.日A』、rG.S^甜一铂煳,E,,;盘iZ:zjza40jjD囝矗,14.∞,雄【Abstract】0bjectiveTostudytheimmunologicmechanisminpathogenesisoftheacutepancreatitis(AP)andtheinterventioneffectsofsandostatinandmagnol01.MethoibNinety
7、BALB/cmiceweredividedintonegativecontrolgroup,caerulein—inducedmodelgroup,sandostatin—treatmentgroup,magnolol—treatmentgroup,combinedsandostatin—andmagnolol—treatmentgroupbymeansofrandomnumbertable,with18miceineachgroup.APmodelwasreproducedbysevenintraper
8、itorlealinjectionsofcaeruleinatanintervalof1hour.Every30minutesbeforethecaeruleinchallenge,sandostatinwasinjectedsub—cutaneously.1订agnololwasinjectedintravenouslyimmediatelyaftertheAPmodelwasreproduced.Thenat9,12,24
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