共查询到20条相似文献,搜索用时 46 毫秒
1.
肝纤维化是一个可逆的动态过程,研发药物抑制、逆转肝纤维化成为治疗慢性肝病的热点问题。本文针对肝纤维化过程中的重要环节,从肝细胞、肝星状细胞和细胞外基质等不同药物作用靶点,对目前抗肝纤维化药物研究进展做一综述。 相似文献
2.
3.
酒精性肝纤维化中肝星状细胞活化的机制研究进展 总被引:3,自引:0,他引:3
赵菁 《国外医学(药学分册)》2006,33(3):198-203
肝星状细胞(HSC)活化是各种病因所致肝纤维化过程中的关键环节。在酒精性肝病的发展过程中,乙醇和代谢产物乙醛可改变机体氧化还原状态,活化枯否细胞,释放大量细胞因子,诱导HSC活化、增殖和胶原合成,形成肝纤维化。本文将对酒精性肝纤维化中HSC活化的机制和相关靶点加以综述,为开发抗肝纤维化药物和临床治疗提供新的思路。 相似文献
4.
肝纤维化(HF)是各种致病原因引起细胞外基质(ECM)在肝内过多沉积的过程,它是大多数慢性肝病所共有的病理特征,是众多慢性肝病发生发展的必经阶段.研究业已证明,肝星状细胞(HSC)在肝纤维化的发生发展过程中发挥关键作用.在损伤因子作用下,HSC增殖、活化,产生细胞外基质(ECM),是肝纤维化发生的关键细胞、重要环节[1].进展性肝纤维化具有一定的可逆性,现就其治疗研究进展综述如下. 相似文献
5.
6.
肝纤维化时肝星状细胞激活因素研究进展 总被引:2,自引:0,他引:2
肝纤维化(liver fibrosis,LF)是指肝细胞发生坏死及炎症刺激时,肝脏中胶原蛋白等细胞外基质(ECM)增生与降解失去平衡,导致肝脏内纤维结缔组织异常沉积的病理过程。在过去的几十年中,对肝纤维化的发生机制及其转归的研究一直是医学界研究的重点,目前肝星状细胞已成为研究LF发生机制中最受重视的细胞。 相似文献
7.
8.
9.
复方861对习肝星状细胞增殖及胶原合成的影响 总被引:9,自引:0,他引:9
目的 观察中药复方861对体外培养肝星状细胞增殖及胶原合成的影响。方法 分离培养大鼠肝星状细胞,传一代后加入不同浓度的复方861作用48小时,以MTT比色法检测对细胞增殖的作用,传一代细胞以10mg/ml复方861作用48小时后,以ELISA法、斑点杂交法检测胶原蛋白分泌及相应mRNA水平的变化。结果 1.56-100mg/ml复方861(经0.45μm滤膜过滤)可使MTT转化率下降,细胞增殖受抑,呈明显的剂量依赖性;10mg/ml复方861可使Ⅰ、Ⅲ、Ⅳ型胶原及转化生长因子β1(TGFβ1)mRNA水平及相应蛋白分泌量下降。结论 复方861抗纤维化的部分机理在于抑制活化肝星状细胞的增殖及胶原蛋白的合成,从而减少胶原纤维在肝脏内的沉积。 相似文献
10.
熊果酸抗实验性大鼠肝纤维化作用机制的研究 总被引:4,自引:0,他引:4
目的观察熊果酸对实验性大鼠肝纤维化的影响及可能的作用机理。方法将不同剂量的熊果酸10mg(kg/d)、20mg(kg/d)、40mg(kg/d)作用于二甲基亚硝胺(DMN)所致肝纤维化大鼠,在药物治疗4周后观察熊果酸对肝纤维化大鼠肝功能的影响;观察熊果酸对氧化指标SOD、MDA的影响;病理学方法观察熊果酸治疗后组织形态学的变化;RT-PCR方法检测熊果酸对MMP-1mRNA、TIMP-1mRNA表达变化。结果熊果酸可明显改善肝纤维化大鼠肝功能,并呈剂量依赖性;不同剂量熊果酸作用4周后能显著增加SOD表达,降低MDA表达;在病理学形态方面,熊果酸治疗组使肝组织结构不同程度改善;不同剂量熊果酸作用4周后RT-PCR方法检测治疗组MMP-1mRNA的表达较模型组相比明显升高,TIMP-1mRNA表达较模型组相比显著降低。结论熊果酸可明显改善肝纤维化大鼠肝功能,并呈剂量依赖性;熊果酸能显著增加SOD表达,降低MDA表达;熊果酸可上调MMP-1mRNA的表达,下调TIMP-1mRNA的表达;熊果酸治疗肝纤维化的作用机制可能与阻断氧化应激过程,抑制脂质过氧化,增加细胞外基质(ECM)的降解,减少ECM的沉积等机制有关。 相似文献
11.
The purpose of this study was to test whether or not the antiviral drug amantadine induces the structural features of lipidosis in intact animals (rats) and cultured cells, and to investigate the interactions between amantadine and phospholipids. Chlorphentermine was used as reference compound. When subchronically fed to rats at a daily dosage of approximately 180 mg/kg, amantadine induced ultrastructural symptoms of generalized lipidosis, the degree of which was, however, by far less marked than that previously reported for chlorphentermine. This was paralleled by the findings on cell cultures (rat peritoneal macrophages), where the lipidosis-inducing potency of amantadine was approximately 10-fold lower than that of chlorphentermine. As to drug-phospholipid interactions, amantadine had less marked effects than chlorphentermine upon the phase transition characteristics of phosphatidylcholine and phosphatidic acid; furthermore, amantadine was approximately 10-fold less potent than chlorphentermine in displacing Ca from phosphatidylserine monolayers. The present study has revealed a parallel between the comparatively low lipidosis-inducing efficacy inherent to amantadine and the comparatively low tendency to interact with phospholipids. It is suggested that the cage-like structure of the amantadine molecule hinders an effective intercalation of the drug into phospholipid aggregates, and that this is an essential factor responsible for the low inherent efficacy of amantadine with respect to lipidosis induction. 相似文献
12.
肝纤维化是大多数慢性肝病所共有的病理特征 ,其本质是肝内细胞外基质合成大于降解而导致过度沉积。胶原是细胞外基质的主要组成成分 ,因此 ,有效抑制胶原的合成、促进胶原降解是抗肝纤维化的一条重要途径。本文就肝纤维化的胶原代谢和抗肝纤维化治疗作一综述。 相似文献
13.
14.
WACHTEL E 《British medical journal》1958,1(5061):20-22
15.
<正>胰腺纤维化(pancreatic fibrosis)是很多胰腺疾病的病理终点,可由急慢性胰腺炎、胰腺肿瘤以及自身免疫性疾病等疾病引发,最终导致胰腺功能的降低至完全损毁。近年来,随 相似文献
16.
17.
肝纤维化的药物治疗研究现状 总被引:1,自引:0,他引:1
肝纤维化是多种慢性肝病(如病毒性肝炎、酒精性肝病、非酒精性脂肪肝、中毒性肝病、自身免疫性肝病等)晚期共有的组织学变化,是肝脏损害后的一种修复过程,可最终导致肝硬化、肝癌等严重疾病。 相似文献
18.
A perspective view on widespread pulmonary fibrosis 总被引:1,自引:0,他引:1
M Turner-Warwick 《British medical journal》1974,2(5915):371-376
19.
E. Autret S. Marchand M. Breteau B. Grenier 《European journal of clinical pharmacology》1986,31(1):79-83
Summary 36 pharmacokinetic studies of amikacin were performed to evaluate the bronchial diffusion of amikacin in 9 children with cystic fibrosis, 3 to 15 years old. Amikacin was administered i.v. according to a variable dosage regimen. Four children without cystic fibrosis were enrolled as controls. The mean half life was 1.1, the volume of distribution averaged 0.26 l/kg, and the mean plasma clearance was 131 ml/min/1.73 m2, which no differed from that of the controls. The mean peak plasma concentration was always above the MIC but its level depended on the unit dose: 18.5 mg/l, 25,95 mg/l and 31,46 mg/l for doses of 5, 7.5 and 12.5 mg/kg, respectively. Between consecutive amikacin infusions, the plasma level was above the MIC for 21% and 46% of the time after the 5 and 7.5 mg/kg doses. The maximum concentration in sputum between H1 and H2 was always below the MIC, except after 15 mg/kg. The ratio AUC sputum/AUC plasma was between 0.028 and 0.61, and it increased from the beginning to the end of the course of treatment. No side effects were observed on hearing, or vestibular and renal function. The results are used to suggest more appropriate dosing regimens. 相似文献
20.