四逆软肝方病证结合治疗肝硬化特色分析

肝硬化为慢性、难治性、不可逆性、高死亡率、顽固性疾病。笔者认为肝硬化的病因病机复杂多样,但始动病因为湿热疫毒,病机为肝肾阴虚、痰瘀互结、本虚标实、虚实夹杂,结合现代医学临床表现及病证分型,在治疗上立足中医整体观、辨证论治,以清热利湿、疏肝健脾、活血化痰、软坚散结、益气养阴为基本大法,创制四逆软肝方治疗肝硬化,临床疗效颇著,实现了肝硬化难以逆转的"四逆"。     

鸡传染性贫血病免疫对肝脏微粒体苯胺羟化酶活性的影响

为了观察鸡传染性贫血病(Chicken Infectious Anemia,CIA)免疫对肝脏微粒体苯胺羟化酶活性的影响。20只70日SPF龄白来航蛋鸡随机分为2组,每组10只。免疫组用鸡传染性贫血病弱毒苗免疫4次,每次间隔2周,对照组鸡注射同剂量的生理盐水。最后一次免疫后10 d取肝脏制备微粒体,测定肝微粒体这苯胺羟化酶的活性。结果表明:免疫组鸡苯胺羟化酶的活性为66.034±2.071 nmol/(mg.min),对照组为141.853±19.310 nmol/(mg.min)。与对照组相比,免疫组苯胺羟化酶的活力极显著下降(P﹤0.01)。鸡传染性贫血病免疫可降低肝脏微粒体苯胺羟化酶的活性。     

铅与维生素C对小鼠肝脏脂质过氧化的影响

以五周龄昆白系小鼠为试验动物,在饲喂小鼠普通日粮基础上每天灌喂一定量铅(Pb)、维生素C(Vc)、Vc Pb,Vc用量200mg/kg,Pb四个浓度分别为1.2g/L、0.4g/L、0.13g/L、0.043g/L,饲喂期三周,检测小鼠肝脏中铅与丙二醛(MDA)含量以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化物酶(POD)的活性变化。结果表明:铅在小鼠肝脏中大量蓄集,并引起MDA含量增加;加Pb组与空白对照组相比SOD酶活性降低,且随着铅浓度的降低而升高;CAT活性测定显示:Pb1、Pb2组与空白对照组相比差异显著(p<0.05),Pb3组差异极显著(p<0.01),除Vc Pb4组与Pb4组相比差异不显著(P>0.05)外,其他Vc Pb组与其对应加Pb组比较,均差异显著(p<0.05);POD活性测定表明:Vc组与空白组相比差异极显著(p<0.01),Pb1、Pb3组与空白组比较差异显著(p<0.05),Pb2、Pb4与空白组比较差异极显著(p<0.01),除Vc Pb1组与Pb1组差异不显著(P>0.05),其他Vc加Pb组与单独加Pb组相比差异极显著(p<0.01)。因此,Pb可增强小鼠肝脏脂质过氧化,而Vc可减轻铅引起的过氧化损伤。     

从肝论治法对白癜风β-EP、CGRP、NPY表达的影响

目的观察从肝论治法治疗寻常型白癜风的临床效果。方法将符合标准的寻常型白癜风患者分为治疗组35例与对照组35例,两组患者均经过2周洗脱期后,治疗组口服复方祛白颗粒,同时外用复方祛白酊治疗。对照组口服白癜风胶囊,同时外用复方祛白酊。治疗3个月后,检测寻常型白癜风患者血浆β-内啡肽（beta～Endorphin,β-EP）、降钙素基因相关肽（calcitoningene--relatedpeptide,CGRP）、神经肽Y（neuropeptideY,NPY）水平。结果与对照组相比,治疗组疗效明显优于对照组（P〈0．05）。与对照组相比,治疗组口～EP、CGRP、NPY水平明显低于对照组（P〈0．05）。结论从肝论治法治疗寻常型白癜风具有较好的临床疗效,β-EP、CGRP、NPY水平的升高很可能是寻常型白癜风发病的重要因素。     

肝硬化并自发性细菌性腹膜炎患者血清和腹水一氧化氮的测定及临床意义

目的 :观察肝硬化并自发性细菌性腹膜炎 (SBP)患者血清和腹水中一氧化氮 (NO)水平的变化及临床意义。方法 :肝硬化腹水 72例分为SBP组 (n =4 0例 )和漏出液组 (n =32例 ) ,采用Gress法测定两组患者血清和腹水的NO的变化。结果 :SBP组血清和腹水的NO水平明显高于漏出液组 (P <0 .0 1 ) ;SBP组腹水NO水平又明显高于血清中的NO水平 ,且随着感染的控制 ,腹水中NO水平明显下降 (P <0 .0 1 )。结论 :腹水NO的检测有助于SBP的诊断和疗效观察     

三种不同给药途径建立小鼠肝硬化模型的比较

按逐步增加食用白酒浓度的方法诱导肝硬化的模型,将80只KM雄性小鼠随机分为4组,A组采用灌胃,B组采用皮下注射,C组采用腹腔注射,D组为对照组,并把20只SD大鼠随机分为皮下注射E组、对照组F组。观察各组的体重变化、死亡率和肝假小叶形成率。采用上述方法诱导7周后A～F组小鼠体重早期缓慢下降,后期缓慢增加。A组死亡5只,死亡率25%,假小叶形成率65.2%;B组死亡1只,死亡率5%,假小叶形成率92.5%;C组死亡2只,死亡率10%,假小叶形成率86.5%;E组大鼠体重早期明显下降,后期缓慢增加,死亡5只,死亡率50%,假小叶形成率66.7%;D组、F组体重明显增加,无死亡,无肝硬化形成。结果表明:小鼠皮下注射给药,逐步增加食用白酒的浓度可以缩短肝硬化形成的时间,提高形成率,降低死亡率。     

茶多酚对小鼠肝DNA甲基化酶活性的影响

采用茶多酚 (TP)处理老年小鼠 ,并用3 H-甲基掺入法测定了成年和老年小鼠肝DNA甲基化酶的活性。以传统抗衰老中药人参作阳性对照 ,结果证明TP和 0 2 %的人参汤剂能明显提高老年小鼠肝细胞DNA甲基化酶的活性 ,具有延缓衰老的作用 ,为从分子生物学角度探讨TP延缓衰老的机理提供了依据     

Changes of liver sinusoidal endothelial cells and basement membrane in early stage of liver fibrosis induced by carbon tetrachloride in rats

AIM：To explore the development of hepatic sinusoidal capillarization in the early stage of liver fibrosis induced by carbon tetrachloride (CCl4) in rats. METHODS：Clean SD rats were randomly divided into normal control group (group N, n=6) and liver fibrotic model group (group M, n=32). The rats in group N were intraperitoneal injected with saline and the rats in group M were intraperitoneal injected with CCl4 (2 mL/kg, twice a week for 4 weeks). At the end of the 3rd day and the 1st, 2nd and 4th weeks, all rats were killed and then the samples were collected. The pathological changes in the livers were observed by HE staining and Masson straining. The development of hepatic sinusoidal capillarization was observed by transmission electron microscopy (TEM) and immunohistochemical staining. The cell surface expression of vascular endothelium-associated marker CD31, collagen type Ⅳ (Col IV) and laminin (LN) was determined. RESULTS：HE and Masson staining showed the formation of liver fibrosis after treatment with CCl4 for 4 weeks. TEM showed that the fenestrate diameter of liver sinusoidal endothelial cells (LSECs) grew down, the fenestrate numbers of LSECs were decreased along with the development of liver fibrosis, and the consecutive basement membrane was formed at the end of the experiment. The expression of CD31 was significantly increased along with the development of defenestration, and the expression of Col IV and LN was significantly increased after the treatment with CCl4 for 2 weeks and 4 weeks, respectively. CONCLUSION：The typical hepatic sinusoidal capillarization was detected in the early stage of liver fibrosis, and the deposition of LN in the liver sinusoidal walls was the mainly factor of formation of the consecutive basement membrane.     

Incidence,Timing, and Risk Factors of Azathioprine Hepatotoxicosis in Dogs

Background

The use of azathioprine (AZA) in dogs is limited by the development of hepatotoxicosis and cytopenias.

Hypothesis and Objectives

To characterize the observed incidence, timing, and risk factors for AZA hepatotoxicosis in dogs treated clinically, and to determine the relationship between the development of hepatotoxicosis and cytopenias.

Animals

Fifty‐two dogs treated with AZA with clinical and biochemical follow‐up, with a subset of 34 dogs available for determination of changes in liver enzyme activities in serum.

Methods

Retrospective medical record review, from January 2009 through December 2013.

Results

Hepatotoxicosis (as defined by a >2‐fold increase in serum ALT) was observed in 5 of 34 dogs (15%) within a median onset of 14 days (range, 13–22 days). Dogs had a median 9‐fold increase in ALT and 8‐fold increase in ALP, which stabilized or resolved with drug discontinuation or dose reduction. German shepherds were significantly over‐represented (3 of 5 dogs with hepatotoxicosis; P = .0017). Thrombocytopenia or neutropenia were seen in 4 of 48 dogs with CBC follow‐up (8% of dogs), but occurred significantly later in treatment (median onset, 53 days; range 45–196 days) compared to hepatotoxicosis (P = .016).

Conclusions and Clinical Importance

These results support the routine monitoring of liver enzymes during the first 1–4 weeks of AZA treatment in dogs, with continued monitoring of the CBC. Additional studies are warranted to characterize the apparently higher risk of AZA hepatotoxicosis in German shepherds.     

Liver fluke isolates: a question of provenance

A survey of literature on experimental infections with the liver fluke, Fasciola hepatica published between 2005 and 2009 has revealed a general lack of information on where fluke material (i.e. metacercariae) was sourced from. Even less information was given on the drug status of the fluke isolate used, which is a particular concern for those studies that involved anthelmintics. In these two respects, information on the liver fluke lags far behind that for nematodes, where such information is given almost as a matter of course. Of additional concern is that, at times, information about the source and drug history of fluke isolates was incorrect. The overall aim of the review is to demonstrate why it is important to provide as much information as possible on what fluke material is being used. It also attempts to correct some of the errors in the literature and gather together what information is available about the provenance of those isolates that have been used in recent experimental studies.