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ID:53271877
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页数:5页
时间:2020-04-17
《穿心莲内酯对小鼠急性四氯化碳肝损伤的保护作用.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、CMYK2204实用医学杂志2014年第30卷第14期穿心莲内酯对小鼠急性四氯化碳肝损伤的保护作用万君叶菊风叶俊郭进强摘要目的:研究穿心莲内酯(AP)对小鼠急性四氯化碳(CCl4)肝损伤的保护作用及其机制。方法:40只小鼠随机分成5组,正常对照组、肝损伤模型组、AP低剂量组(50mg/kg)、高剂量组(100mg/kg)和阳性药物组。分别测定小鼠血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)含量;肝匀浆中丙二醛(MDA)、还原型谷胱甘肽(GSH)的含量及肝组织病理学变化;逆转录PCR(RT鄄PCR)检测小鼠
2、肝脏中肿瘤坏死因子α(TNF鄄α)、血红素加氧酶-1(HO鄄1)mRNA水平。结果:AP高剂量组(100mg/kg)降低小鼠血清中ALT、AST水平,提高肝组织中GSH活性,降低MDA水平,差异均有统计学意义(P<0.05);病理镜检显示AP高剂量组明显减轻肝损伤;RT鄄PCR结果显示,AP高剂量组TNF鄄α表达水平降低,而HO鄄1表达增强,差异均有统计学意义(P<0.05)。结论:AP通过抑制脂质过氧化反应,降低组织中氧自由基的生成保护急性四氯化碳肝损伤,其机制可能与抑制TNF鄄α的表达,诱导HO鄄1表达有关。关键词穿心莲
3、内酯;四氯化碳;肝损伤RoleofandrographolideinprotectionofCCl鄄inducedacuteliverinjuryinmiceWANJun鄢,YEJu鄄feng,4YEJun,GUOJin鄄qiang.鄢ExperimentalTeachingCenterofPreventiveMedicine,SchoolofPublicHealthandTropicalMedicine,SouthernMedicalUniversity,Guangzhou510515,ChinaCorresponding
4、author:GUOJin鄄qiangE鄄mail:gwh@fimmu.com【Abstract】ObjectiveToinvestigatetheroleofandrographolide(AP)inprotectionofcarbontetrachloride(CCl4)鄄inducedacuteliverinjuryinmiceandthepossiblemechanisms.MethodsThemicewererandomlydividedintofivegroups,includingtwogroupswithdi
5、fferentdosesofAP(50mg/kgand100mg/kg),acontrolgroup,aCCl4modelgroup,andasilymaringroup.Serumlevelsofalanineaminotransferase(ALT),aspartateminotransferase(AST),hepaticmalondialdehyde(MDA),andglutathione(GSH)wereexamined.Pathologicalchangesintheliverwereobserved.RT鄄PC
6、Rwasusedtodetecttheexpressionsoftumornecrosisfactor鄄a(TNF鄄α)andhemeoxygenase鄄1(HO鄄1)mRNA.ResultsAscomparedwithCCl4modelgroup,serumlevelsofALTandASTandhepaticMDAactivityweresignificantlydecreasedinAPgroup(100mg·kg鄄1),alongwitharemarkableincreaseinhepaticGSHcontent.P
7、retreatmentwithAPatahighdosealleviatedhistopathologicalchangesinducedbyCCl4.AmarkedlyincreasedlevelofTNF鄄ainducedbyCCl4wasreducedbyAP,whileHO鄄1attranscriptionallevelwasdramaticallyelevatedfollowingAPpretreatment.ConclusionsAPplaysaroleinprotectionofCCl4鄄inducedacut
8、eliverinjurybyinhibitinglipidperoxidationandreducingformationoffreeradicals,themechanismmaybeinvolvedininhibitionofTNF鄄αandactivationofHO鄄1.【Keyw
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