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《壳聚糖介导CrmA基因治疗小鼠肝纤维化的研究-论文.pdf》由会员上传分享,免费在线阅读,更多相关内容在应用文档-天天文库。
1、现代生物医学进展www.shengwuyixue.comProgressinModernBiomedicineVoL14NO.9MAR.2014·1601·doi:10.13241/j.cnki.pmb.2014.09.001·基础研究·壳聚糖介导CrmA基因治疗小鼠肝纤维化的研究米张新胜卫张宏玲0郑义黄来强’2△(1清华大学生命科学学院北京100084;2清华大学深圳研究生院生命与健康学部生物医药研究中心和基因与抗体治疗重点实验室广东深圳518055)摘要目的:探讨壳聚糖介导的CrmA对小鼠肝纤维化的治疗效果,以期为肝纤维化的基因治疗提供实验基础。方法:清洁级的75只雄性小鼠随机分为正常组
2、、模型组、壳聚糖介导的CrmA组、壳聚糖介导的空载体组、壳聚糖组,每组15只。应用30%四氯化碳橄榄油溶液3ml/kg腹腔注射制备肝纤维化小鼠模型。治疗8周后,眼眶取血,检测血清的肝功能指标,并取肝组织做HE染色,观察各组小鼠肝脏的病理形态,RealTimePCR检测肝组织儿-113、0【一SMA、TGF.131、TIMP.1表达量。结果:与模型组小鼠相比,壳聚糖介导的CrmA组小鼠的肝纤维化程度减轻,ALT、AST显著降低(P3、壳聚糖介导的CrmA能有效减轻肝纤维化小鼠的肝脏损伤和纤维化程度,为基因治疗肝纤维化提供了一种潜在的新思路和方法。关键词:肝纤维化;细胞因子反应调节蛋白A;白介素.1B;壳聚糖;基因治疗中图分类号:Q782,R966,R575.2文献标识码:A文章编号:1673-6273(2014)09—1601.05GeneTherapyforMouseHepaticFibrosiswithChitosan.mediatedCrmA*zHANGXin-sheng‘,ZHNGHong-ling~'e,ZHENGYgHUANGLai-qiangJe~《lSchoolofLifeSciences,Tsinghu4、aUniversity,Beijing,100084,China;2TheShen~enKeyLabofGeneandAntibodyTherapy,CenterforBiotech&BioMedicineandDivisionofLife&HealthSciences,GraduateSchoolatShenlJlen,TsinghuaUniversity,Shenzhen,Guangdong,518055,China)ABSTRACTObjective:Toexplorethetherapeuticefectsofthechitosan-·mediatedCrmAonCC14-induc5、edhepaticfibrosisinmouse.Methods:Seventyfivemalemiceofcleangradeweredividedevenlyintofivegroupsmarked”Normal”,”Model”,”chitosan—me—diatedCrmA”.”chitosan—mediatedvector”and”Chitosan”.Liverfibrosismodelmiceweregiven30%carbontetrachlorideoliveoilsolution3ml/kgbyintraperitonealinjection.Aftereightweeks6、oftreatment,hepaticfibrosiswasevaluatedthroughmeasuringserumALTandAST,examiningHEpigmentation,anddeterminingbyRealTimePCRtheexpressionlevelsofIL—lB,or,一SMA,TGF一131andTIMP一1inhepatictissue.Results:Comparedwiththemodelgroup,thedegreeofliverfibrosisinthechitosan-mediatedCrmAgroupwasobviouslyreduced.Th7、eALTandASTlevelsofthechitosan—mediatedCrmAgroupweremuchlowerthanthatofmodelgrouprP<0.01).ThemRNAexpressionof1L一113,仅一SMAandTIMP-1wasreducedmarkedlyinthechitosan—mediatedCrmAgroup(P<0.05),ascomparedwiththemo
3、壳聚糖介导的CrmA能有效减轻肝纤维化小鼠的肝脏损伤和纤维化程度,为基因治疗肝纤维化提供了一种潜在的新思路和方法。关键词:肝纤维化;细胞因子反应调节蛋白A;白介素.1B;壳聚糖;基因治疗中图分类号:Q782,R966,R575.2文献标识码:A文章编号:1673-6273(2014)09—1601.05GeneTherapyforMouseHepaticFibrosiswithChitosan.mediatedCrmA*zHANGXin-sheng‘,ZHNGHong-ling~'e,ZHENGYgHUANGLai-qiangJe~《lSchoolofLifeSciences,Tsinghu
4、aUniversity,Beijing,100084,China;2TheShen~enKeyLabofGeneandAntibodyTherapy,CenterforBiotech&BioMedicineandDivisionofLife&HealthSciences,GraduateSchoolatShenlJlen,TsinghuaUniversity,Shenzhen,Guangdong,518055,China)ABSTRACTObjective:Toexplorethetherapeuticefectsofthechitosan-·mediatedCrmAonCC14-induc
5、edhepaticfibrosisinmouse.Methods:Seventyfivemalemiceofcleangradeweredividedevenlyintofivegroupsmarked”Normal”,”Model”,”chitosan—me—diatedCrmA”.”chitosan—mediatedvector”and”Chitosan”.Liverfibrosismodelmiceweregiven30%carbontetrachlorideoliveoilsolution3ml/kgbyintraperitonealinjection.Aftereightweeks
6、oftreatment,hepaticfibrosiswasevaluatedthroughmeasuringserumALTandAST,examiningHEpigmentation,anddeterminingbyRealTimePCRtheexpressionlevelsofIL—lB,or,一SMA,TGF一131andTIMP一1inhepatictissue.Results:Comparedwiththemodelgroup,thedegreeofliverfibrosisinthechitosan-mediatedCrmAgroupwasobviouslyreduced.Th
7、eALTandASTlevelsofthechitosan—mediatedCrmAgroupweremuchlowerthanthatofmodelgrouprP<0.01).ThemRNAexpressionof1L一113,仅一SMAandTIMP-1wasreducedmarkedlyinthechitosan—mediatedCrmAgroup(P<0.05),ascomparedwiththemo
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