1) immunological hepatic fibrosis
免疫性肝纤维化
1.
Effects of total glucosides of paeony on protein expression of NF-kappa B and TGF-β1 in hepatic tissue of rats with immunological hepatic fibrosis;
白芍总苷对免疫性肝纤维化大鼠肝组织NF-κB和TGF-β1蛋白表达的影响
2.
Objective To investigate the effects of SQDG on Bacillus Calmette Guerin (BCG) plus lipopolysaccharide(LPS)-induced immunological liver injury in mice as well as its possible mechanisms, to study the therapeutic effects and mechanisms of SQDG on immunological hepatic fibrosis induced by human albumin in rats .
目的:探讨芍芪多苷(SQDG)对卡介苗(Bacillus Calmette Guerin,BCG)加脂多糖(lipopolysaccharide,LPS)诱导的小鼠免疫性肝损伤模型的保护作用及SQDG对人白蛋白致免疫性肝纤维化大鼠模型的抗肝纤维化作用并对其机制作初步研究。
3.
Objective To study the effects and mechanisms of total glucosides ofpaeony (TGP) on immunological hepatic fibrosis induced by human albumin in rats .
目的：探讨白芍总苷(total glucosides of paeony，TGP)对人白蛋白致大鼠免疫性肝纤维化模型的作用及其部分机制。
2) immuno-hepatic fibrosis
免疫性肝纤维化
1.
Objective:To study the expression and significance of insulin-like growth factor–1(IGF-1) and its intervention by rosiglitazone in immuno-hepatic fibrosis rats, and to clarify the relationship between IGF-1 and hepatic fibrogenesis.
目的探讨大鼠免疫性肝纤维化时胰岛素样生长因子-1(IGF-1)的表达变化及意义,观察过氧化物酶体增生物激活受体γ(PPARγ)的配体─罗格列酮对其表达的影响,研究其与肝纤维化发生、发展的关系,为肝纤维化的诊治提供实验室依据。
2.
Objective:To study the expression and signification of peroxisome proliferator activated receptorγ(PPARγ)and its intervention by rosiglitazone in immuno-hepatic fibrosis rats,and to clarify the relationship between PPARγand hepatic fibrogenesis.
目的探讨大鼠免疫性肝纤维化时过氧化物酶体增殖物激活受体γ(PPARγ)的表达变化及意义,观察过氧化物酶体增殖物激活受体γ(PPARγ)的配体—罗格列酮对其表达的影响,研究其与肝纤维化发生、发展的关系,为肝纤维化的诊治提供实验室依据。
3) immune fibrosis
免疫性肝纤维化
1.
Effect of gypenosides on hepatic function and fibrosis in rats with immune fibrosis;
绞股蓝总皂苷对免疫性肝纤维化大鼠肝功能和肝纤维化的影响
4) liver fibrosis/Immune
肝纤维化/免疫性
5) Immunological fibrosis of liver
免疫性损伤性肝纤维化
6) immunity-damaged liver fibrosis model
免疫损伤性肝纤维化模型
补充资料：肝外阻塞性胆汁性肝硬化
肝外阻塞性胆汁性肝硬化
又称"继发性胆汁性肝硬化。*胆汁性肝硬化的一个类型，继发于肝外胆管阻塞而引起的肝硬化。主要由总胆管结石、手术后胆管狭管、胰头癌、先天性胆管闭锁或缺如等原因所造成。在梗阻上端的胆道由下而上地逐渐扩大迂曲，胆汁淤积，肝内小胆管扩大而破裂，使肝血管受压，胆汁外渗，肝细胞发生缺血、坏死，纤维组织增生，最后形成肝硬化。临床表现为黄疸、肝脾肿大，皮肤粘膜出血倾向，血胆固醇下降等，晚期表现同*肝硬化。解除肝外阻塞原因，本病有治愈的可能性。
说明：补充资料仅用于学习参考，请勿用于其它任何用途。
参考词条