18α-和18β-甘草酸治疗肝病的疗效比较

18α-甘草酸是18β-甘草酸的差向异构体,二者对急、慢性免疫性肝损伤和多种化学性急、慢性肝损伤动物模型均有显著的肝脏保肝作用,临床上治疗各种类型的肝病(包括重症、急、慢性病毒性肝炎和化学性肝病以及肝纤维化)均有效。综述了18α-甘草酸与18β-甘草酸在治疗病毒性肝炎、肝纤维化以及其他肝病的作用,并作了临床疗效比较,发现18α-甘草酸(甘草酸二铵)优于国产的18β-甘草酸(甘草酸单铵),但弱于日本产的18β-甘草酸(甘草酸苷)。     

复方甘草酸苷治疗慢性乙型肝炎疗效观察

为进一步探讨复方甘草酸苷(美能)的疗效,我院应用美能治疗慢性乙型病毒性肝炎,取得满意疗效,现报告如下。1.资料与方法1.1一般资料82例患者均为我院2004年6月￣2005年5月的住院病例,全部病例诊断符合2002年(南京)第10次全国病毒性肝炎与肝病学术会议修订的《病毒性肝炎防治方案》的诊断标准,且符合下列条件:所有病例HBVDNA ,并排除心、脑、肺、肾等基础疾病,无合并甲、丙、丁、戊型病毒性肝炎,无酒精性、药物性、代谢性或自身免疫性肝病。82例随机分为治疗组(复方甘草酸苷组)和对照组(门冬氨酸钾镁治疗组)。治疗组42例(男32例,女10例),年…     

异甘草酸镁治疗慢性乙型肝炎疗效观察

目的探讨异甘草酸镁治疗慢性乙型病毒性肝炎的临床疗效及不良反应。方法 15例慢性乙型肝炎患者随机分为异甘草酸镁组和对照组,分别予异甘草酸镁常用剂量治疗及甘草酸二铵治疗,观察各组治疗效果及不良反应出现情况,并进行比较。结果异甘草酸镁组临床症状改善及肝功能指标改善明显,与对照组比较差别有统计学意义(P<0.05),而不良反应轻微,且其发生与对照组比较有统计学差异(P<0.05)。结论与甘草酸二铵相比,异甘草酸镁治疗慢性乙型病毒性肝炎疗效更显著,不良反应更小,值得进一步探讨研究。     

抗丙型肝炎病毒常用药物

丙型病毒性肝炎(丙肝)呈全球性流行趋势,致病的根本原因是丙型肝炎病毒(HCV)感染。丙肝的病理改变与乙型病毒性肝炎相似,以肝细胞坏死和淋巴细胞浸润为主。丙肝慢性化可导致肝脏慢性炎症坏死和纤维化,部分患者可发展为肝硬化甚至肝细胞癌,对患者的健康和生命危害极大。目前,丙肝治疗已经取得长足的进展,可治疗丙肝、丙肝相关肝病和合并其他疾病的患者。本文主要对丙肝的流行特点、HCV特点及抗HCV常用药物如干扰素、索磷布韦、索磷布韦/维帕他韦等进行概述。     

贺普丁治疗慢性乙型肝炎的不良反应及护理

慢性乙型病毒性肝炎(以下简称乙肝)治疗的最佳方案是抗病毒治疗,约88%的慢性乙肝患者需要长期抗病毒治疗已成为共识。2010版《慢性乙型病毒性肝炎防治指南》指出:慢性乙肝治疗的总体目标为最大限度地长期抑制或消除乙型肝炎病毒(HBV),减轻肝细胞炎症坏死及纤维化,延缓和阻止疾病进展,减少和防止肝脏失代偿、肝硬化、原发性肝癌(HCC)及其并发症的发生,从而改善生活质     

乙型病毒性肝炎抗病毒类治疗药物研究进展

目前,乙型病毒性肝炎已经引起世界性的广泛关注,而我国又是世界上感染乙型肝炎病毒人数最多的国家,因此,乙型病毒性肝炎治疗药物备受瞩目。现用于治疗慢性乙型病毒性肝炎的药物主要有核苷类似物、干扰素和免疫调节剂3大类。该文对已经上市的乙型病毒性肝炎治疗药物的研究情况进行了简单介绍。     

肝病用药的合理选用

肝病是指发生在肝脏的病变,包括病毒性肝病如甲型病毒性肝炎、乙型病毒性肝炎、丙型病毒性肝炎,以及脂肪肝、酒精肝、肝硬化、药物性肝损伤等多种疾病。中医学的肝病是指肝(包括胆)的生理功能及肝胆经络病理变化所表现出的一切病证的总称。中医对肝病的治疗,需要根据中医药理论辨病、辨证相结合地合理用药。现就中成药在肝病治疗中的作用以及辨证用药简介如下。1中药在肝病治疗中的作用1.1具有降低转氨酶作用的中成药     

异甘草酸镁联合茵栀黄治疗慢性乙型病毒性肝炎40例

目的 评价异甘草酸镁的临床效果及安全性.方法 将84例慢性乙型病毒性肝炎患者随机均分为两组,治疗组(42例)应用异甘草酸镁联合茵栀黄注射液,对照组(42例)应用甘草酸二铵联合茵栀黄,治疗结束后进行疗效评估.结果 丙氨酸氨基转移酶(ALT)及血清胆红素(TBIL)复常的有效率治疗组分别为90.48%和80.95%.对照组分别为88.10%和69.05%,两组差异有显著性(P＜0.05).两组治疗均出现不良反应,各2例(4.76%),不良反应率无显著性差异(P＞0.05).结论 异甘草酸镁在慢性乙型病毒性肝炎治疗中有较好的疗效.     

病毒性肝炎的病原学分型及诊断依据

1　病原学分型目前病毒性肝炎的病原学分型至少可分为六型 ,即甲型病毒性肝炎 (HAV)、乙型病毒性肝炎 (HBV)、丙型病毒性肝炎(HCV)、丁型病毒性肝炎 (HDV)、戊型病毒性肝炎 (HEV)和庚型病毒性肝炎 (HGV)。2　各型病毒性肝炎病原学诊断依据2.1　甲型肝炎　急性肝炎患者血清抗 HAVIg M阳性 ,可确诊为近期感染。但在慢性乙型肝炎或自身免疫性肝病患者 ,血清中检测抗 HAVIg M阳性时 ,判断 HAV重叠感染应慎重 ,需排除类风湿因子 (RF)及其他原因引起的假阳性。接种甲型肝炎疫苗后 2～ 3周约 8%～ 2 0 %接种者可产生抗 - HAVIg M,…     

慢性乙型病毒性肝炎临床治疗探讨

慢性乙型病毒性肝炎（Chronic Viral Hepatitis B,CHB）简称慢性乙肝,是由乙型肝炎病毒（HBV）引起的传染病。本病在我国广泛流行,人群感染率高,严重危害了人民的健康。本文着重探讨慢性乙型病毒性肝炎临床治疗,现报告如下。     

The pharmacokinetics of glycyrrhizic acid evaluated by physiologically based pharmacokinetic modeling

Glycyrrhizic acid is widely applied as a sweetener in food products and chewing tobacco. In addition, it is of clinical interest for possible treatment of chronic hepatitis C. In some highly exposed subjects, side effects such as hypertension and symptoms associated with electrolyte disturbances have been reported. To analyze the relationship between the pharmacokinetics of glycyrrhizic acid in its toxicity, the kinetics of glycyrrhizic acid and its biologically active metabolite glycyrrhetic acid were evaluated. Glycyrrhizic acid is mainly absorbed after presystemic hydrolysis as glycyrrhetic acid. Because glycyrrhetic acid is a 200-1000 times more potent inhibitor of 11-beta-hydroxysteroid dehydrogenase compared to glycyrrhizic acid, the kinetics of glycyrrhetic acid are relevant in a toxicological perspective. Once absorbed, glycyrrhetic acid is transported, mainly taken up into the liver by capacity-limited carriers, where it is metabolized into glucuronide and sulfate conjugates. These conjugates are transported efficiently into the bile. After outflow of the bile into the duodenum, the conjugates are hydrolyzed to glycyrrhetic acid by commensal bacteria; glycyrrhetic acid is subsequently reabsorbed, causing a pronounced delay in the terminal plasma clearance. Physiologically based pharmacokinetic modeling indicated that, in humans, the transit rate of gastrointestinal contents through the small and large intestines predominantly determines to what extent glycyrrhetic acid conjugates will be reabsorbed. This parameter, which can be estimated noninvasively, may serve as a useful risk estimator for glycyrrhizic-acid-induced adverse effects, because in subjects with prolonged gastrointestinal transit times, glycyrrhetic acid might accumulate after repeated intake.     

Inhibition of nuclear factor kappaB is associated with neuroprotective effects of glycyrrhizic acid on glutamate-induced excitotoxicity in primary neurons

Glycyrrhizic acid is an herbal drug with a broad spectrum of antiviral activities and pharmacological effects and multiple sites of action. We investigated whether glycyrrhizic acid protects against glutamate-induced excitotoxicity and the underlying mechanisms. We found that glycyrrhizic acid protected against neurotoxicity in rat primary neuronal cultures and hippocampal slices by suppression of the glutamate-induced apoptosis. Glycyrrhizic acid conferred neuroprotective properties in a concentration-dependent manner, as determined by cell survival, apoptosis, and Ca(2+) influx. Glycyrrhizic acid selectively inhibited the Ca(2+) influx activated through N-methyl-D-aspartate (NMDA) receptor by glutamate, but not through membrane depolarization elicited by high K(+) induction. Glycyrrhizic acid treatment also diminished glutamate-induced DNA fragmentation and cleavage of poly (ADP-ribose) polymerase (PARP). Electrophoretic mobility shift assay (EMSA) indicated that glycyrrhizic acid inhibited the binding activity of nuclear factor kappaB (NF-kappaB) to its target elements. Western blot analysis of NF-kappaB inhibitor (IkappaBalpha) protein revealed that the inhibitory effect of glycyrrhizic acid on glutamate-induced activation of NF-kappaB activity was attributable to the inhibition of IkappaB kinase activity. Thus, the site of action of glycyrrhizic acid could be a downstream consequence of Ca(2+)entry through NMDA receptors and that NF-kappaB may be one downstream target in this process. These observations suggest that glycyrrhizic acid may be of therapeutic value for the prevention of cerebral damage elicited by the glutamate.     

甘草酸类药物在药物性肝病治疗中的应用

随着新型药物相继大量上市和各种天然药物在临床的广泛应用,药物性肝病(DILD)的发病率逐年增高.甘草酸类药物是临床常用的保肝药物,其用于治疗DILD已取得较好疗效,在DILD的预防与治疗中应用前景良好.本文简要综述甘草酸类药物用于DILD治疗的作用机制.     

Physiologically based pharmacokinetic modeling of glycyrrhizic acid, a compound subject to presystemic metabolism and enterohepatic cycling

Glycyrrhizic acid is currently of clinical interest for treatment of chronic hepatitis. It is also applied as a sweetener in food products and chewing tobacco. In some highly exposed subgroups of the population, serious side effects such as hypertension and electrolyte disturbances have been reported. In order to analyze the health risks of exposure to this compound, the kinetics of glycyrrhizic acid and its active metabolites were evaluated quantitatively. Glycyrrhizic acid and its metabolites are subject to complex kinetic processes, including enterohepatic cycling and presystemic metabolism. In humans, detailed information on these processes is often difficult to obtain. Therefore, a model was developed that describes the systemic and gastrointestinal tract kinetics of glycyrrhizic acid and its active metabolite glycyrrhetic acid in rats. Due to the physiologically based structure of the model, data from earlier in vitro and in vivo studies on absorption, enterohepatic cycling, and presystemic metabolism could be incorporated directly. The model demonstrates that glycyrrhizic acid and metabolites are transported efficiently from plasma to the bile, possibly by the hepatic transfer protein 3-alpha-hydroxysteroid dehydrogenase. Bacterial hydrolysis of the biliary excreted metabolites following reuptake of glycyrrhetic acid causes the observed delay in the terminal plasma clearance of glycyrrhetic acid. These mechanistic findings, derived from analysis of experimental data through physiologically based pharmacokinetic modeling, can eventually be used for a quantitative health risk assessment of human exposure to glycyrrhizic acid containing products.     

甘草酸防治肝损伤药理作用的研究进展

近年来国内外对甘草酸肝损伤的研究证实了甘草酸具有抗病毒、抗感染和调节机体免疫功能、、的作用(glycyrrhizic acid,GL)防治抗氧化应激抑制肝细胞凋亡和促进肝细胞再生。笔者综述了近年来甘草酸在体内外实验动物模型中,抗四氯化碳(CCl4)、D-氨基半乳糖、脂多糖,抗肝纤维化与其他类型的急性肝损伤防治等方面的药理研究进展。     

甘草酸及其衍生物的抗炎和抗变态反应研究进展

甘草酸是甘草的有效成分,其选择性诱导成熟的T淋巴细胞凋亡,调节淋巴细胞数量和功能,纠正外周血T淋巴细胞亚群的紊乱,具有抗炎、抗变态反应的药理作用;其机制为抑制抗体(IgG、IgE)生成,多靶点地抑制补体系统,抑制炎性细胞因子和炎症介质生成,以及对抗炎症介质的致炎作用.综述了近年来国内外对甘草酸及其衍生物抗炎、抗变态反应...     

甘草酸协同麻黄碱的平喘作用机制研究

目的：探讨甘草酸协同麻黄碱的平喘作用机制。方法：利用基于CHO细胞的β2肾上腺素受体（β2-AR）激动药活性评价体系,豚鼠离体气管收缩和组胺引喘的活体动物模型观察甘草酸和麻黄碱联用的协同平喘效果。结果：甘草酸自身不能引起离体气管平滑肌舒张,平喘效果也不显著,但与麻黄碱联用可以通过提高β2-AR的激动效果,明显增强平喘效果。结论：甘草酸通过调节β2-AR信号通路增强麻黄碱的作用效果,两者联用有良好的协同作用。     

甘草酸及其苷元甘草次酸的糖皮质激素样作用

甘草酸在体内水解成甘草次酸,因此甘草酸是甘草次酸的前体药物,而甘草次酸的药理作用强于甘草酸.甘草次酸的化学结构类似于甾体激素.甘草次酸和甘草酸是甾体激素代谢失活酶抑制剂,可提高内源性和外源性糖皮质激素的活性.甘草次酸和甘草酸义町作为配体,与糖皮质激素受体结合,由于甘草次酸和甘草酸的糖皮质激素受体激动活性远低于糖皮质激素...     

复方甘草酸苷注射液联合前列地尔治疗急性黄疸型肝炎疗效研究

目的观察复方甘草酸苷注射液联合前列地尔治疗急性黄疸型肝炎疗效。方法将120例急性黄疸型肝炎患者分为2组,治疗组62例在常规治疗的基础上应用复方甘草酸苷注射液联合前列地尔,对照组58例患者在常规治疗的基础上给予门冬氨酸钾镁注射液。疗程为4周。结果治疗结束时治疗组临床症状、肝功能指标等明显好于对照组（P〈0.05）。结论复方甘草酸苷注射液联合前列地尔能有效治疗急性黄疸型肝炎,安全性良好。     

反相高效液相色谱法测定甘草酸脂质体中甘草酸的含量

目的:建立以反相高效液相色谱法测定甘草酸脂质体中甘草酸含量的方法。方法:色谱柱为Shim-PackVP-ODS,流动相为甲醇-磷酸盐缓冲液(pH=2.6,68∶32),检测波长为254nm,流速为1ml/min。结果:甘草酸与辅料及溶剂峰分离良好;甘草酸检测浓度在1～100μg/ml范围内线性关系良好(r=0.9999,n=5);平均回收率为97.56%(RSD=1.03%)。结论:本法准确、灵敏,可用于甘草酸脂质体中甘草酸的含量测定。