荔枝核总黄酮预防大鼠肝纤维化的初步分析-preliminary analysis of total flavonoids from litchi seeds in preventing hepatic fibrosis in rats.docxVIP
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荔枝核总黄酮预防大鼠肝纤维化的初步分析-preliminary analysis of total flavonoids from litchi seeds in preventing hepatic fibrosis in rats
ThepreliminaryresearchoftotalflavonefromLitchichinensisSonnpreventratshepaticfibrosisABSTRACTObjective:ToobservetheprophylacticeffectoftotalflavonefromLitchichinensisSonn(TFL)onratshepaticfibrosisandapoptosisofactivatedhepaticstellatecells(HSCs)intheliversandtodiscusstherelationshipbetweentheprophylacticeffectsandactivatedHSC.Methods:Aratmodelofhepaticfibrosiswasestabishedbyintraperitonealinjectionofdimethylnitrosamine.TFLwasorallygiventofibroticratsatadoseof100mgor200mg/(kg·d).colchicinewasusedasapositivecontrol.After6weeks,allratsweresacrificedandtheirleftliverlobeswereexaminedhistopathologically.ThedegreesoffibrsiswereevaluatedbyH.EandMassonstrainings;SerumTraillevelsofhyaluronicacid(HA),laminin(LN)andprocollagentypeⅢ(PCⅢ)weremeasuredbyradiommunoassay(RIA);TUNEL-a-SMAmethodswasusedtodetetptosisofHSCtheapoptosis.Results:SerumTraillevelsofHA,LNandPCⅢweresignificantlylowerinthehigh-doseTFLgroupandthaninthecolchicinegroup(allP0.05).Degreeofhepaticliversinthehigh-dosegroupwerealllesssevereincomparisonwiththoseofthecontrolgroupandtheapoptosisratesofHSCwereincreased.Conclusions:TELatadoseof200mg/(kg·d)caninhibittheexpressionofHA,LNandPCⅢ,induceHSCsapotosisandimprovethedegreeoffibrosis,Whichhassomecorrelationwithdose.KeyWords:flavonefromLitchichinensisSonn;Hepaticfibrosis;Hepaticstellatecell英汉缩略词对照表英文缩写HF英文全称Hepaticfibrosis中文全称肝纤维化HSCTFLHepaticstellatecellTotalflavonefromLitchichinensisSonn肝星状细胞荔枝核总黄酮α-SMADMNAlpha-smoothmuscleaortaDimethynitrosamine平滑肌肌动蛋白二甲基亚硝铵ColHALNPCⅢcolchicinehyaluronicacidlaminintypeⅢprocollagen秋水仙碱透明质酸层粘连蛋白Ⅲ型前胶原前言肝纤维化其实质是肝内以胶原为主的肝脏细胞外基质(ECM)各成分合成增多,降解相对不足,致使ECM在肝内过多沉积。肝纤维化没有特定的病因,凡是可以造成肝脏慢性、持续性损伤的疾病,都能启动肝纤维化进程。目前认为ECM累积所形成的肝纤维化通过有效的治疗是可以逆转的,因此,如何有效地防治肝纤维化,已经成为国内外研究的热点。现用于研究肝纤维化动物主要有以下几种:化学性损伤肝纤维化模型、酒精性肝纤维化动物模型、免疫性损伤肝纤维化模型、胆管结扎性肝纤维化动物模型、营养性肝纤维化动物模型、其它肝纤维化动物模型。二甲基亚硝胺(DMN)是一种具有肝毒性和细胞毒性的诱导剂,DMN致肝纤维化的机理,主要是DMN经微粒体转化,引起核酸与蛋白质的甲基化从而导致肝细胞坏死,刺激合成细胞外基质,形成纤维化[1]。DMN法多以腹腔注射途径造模。造模周期短,大鼠死亡率较低,形成的纤维化比较稳定,不易吸收,且与人类肝硬化早期改变及胶原沉积相似[2]。另外,早期形成门脉压增高是DMN法造模的一个重要特征,这与人
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