软肝灵对肝纤维化小鼠肝组织病理学及抗脂质过氧化作用的影响

目的探讨软肝灵对四氯化碳(CCl4)所致肝纤维化小鼠的影响。方法采用CCl4复制肝纤维化小鼠模型,60只昆明种小鼠分为模型组、对照组、软肝灵高、中、低剂量组、秋水仙碱组,每组10只。给药6周后检测小鼠血清中的丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、超氧化物歧化酶(SOD)、丙二醛(MDA)、总蛋白(TP)、白蛋白(ALB)及羟脯氨酸(Hyp),并观察小鼠肝组织病理改变。结果模型组造模6周时ALT、AST、MDA、Hyp水平较对照组升高,SOD、TP及ALB的水平较对照组降低;病理检查提示模型组小鼠肝细胞变性、坏死严重,肝组织损害明显。软肝灵具有剂量依赖性地降低CCl4致小鼠肝损伤血清ALT、AST、MDA、Hyp水平升高(P<0.01)的功能,并能显著升高血清中SOD、TP及ALB的水平而达到延缓肝纤维化进程的作用。同时病理检查也提示,软肝灵中、高剂量组可明显减轻CCl4所致的小鼠肝细胞变性、坏死及肝组织损害程度。结论软肝灵具有延缓CCl4所致肝纤维化进程的作用。     

护肝降酶口服液对四氯化碳所致小鼠慢性肝损伤的保护作用

目的:观察护肝降酶口服液(Hugan Jiangmei oral medicinal liquid,HGJM)对四氯化碳(CCl4)所致小鼠慢性肝损伤的保护作用。方法:以CCl4诱发小鼠慢性肝纤维化模型,采用灌胃法给予HGJM,测定小鼠血清丙氨酸氨基转移酶(ALT)、天门冬酸氨基转移酶(AST)及肝组织病理改变。结果:HGJM在给药8周后,显著降低血清ALT和AST水平,减轻了肝脏的病理损伤。结论:HGJM对CCl4致小鼠的慢性肝损伤有一定的肝保护作用。     

黄花远志根和叶提取物对急性肝损伤小鼠的保护作用

目的：研究黄花远志根和叶提取物对四氯化碳（CCl4）所致急性肝损伤小鼠的保护作用。方法：采用 CCl4诱导化学性急性肝损伤模型,测定小鼠肝脏指数、血清丙氨酸氨基转移酶（ALT）和天门冬氨酸氨基转移酶（AST）,观察小鼠肝脏病理学变化。结果：黄花远志根（4 g、2 g 生药／ kg）和叶（4 g、2 g 生药／ kg）提取物能显著降低 CCl4致小鼠急性肝损伤ALT 和 AST 的升高,明显改善 CCl4对肝组织的病理损伤。结论：黄花远志根和叶对 CCl4致小鼠急性肝损伤具有保护作用。     

三七对四氯化碳肝损伤小鼠的保护作用及形态学研究

目的：研究三七对CCl4肝损伤小鼠的保护作用及形态学变化。方法：采用CCl4复制小鼠肝损伤模型，测定血清丙氨酸氨基转移酶(ALT)、天门冬酸氨基转移酶(AST)、白蛋白(Alb)、计算A／G比值，并采用光镜、电镜观察组织学变化。结果：与CCl4模型组相比，用三七处理后，ALT、AST均显著降低，Alb增加，并能明显改善肝脏组织病理变化和超微结构变化。结论：三七对CCl4致小鼠肝损伤具有保护作用。     

藤茶双氢杨梅树皮素对实验性慢性肝损伤的保护作用

目的：探讨从藤茶提取的双氢杨梅树皮素（APS）对慢性肝损伤的保护作用。方法：采用四氯化碳（CCl4）建立小鼠慢性肝损模型，并给予APS观察其对实验鼠血清丙氨酸氨基转移酶（ALT），天门冬氨酸氨基转移酶（AST）活性，总蛋白（TP），白蛋白（ALB），透明质酸（HA）含量和肝组织羟脯氨酸（HyP）含量的影响及肝组织病理改变的影响。结果：APS明显降低血清ALT，AST活性，血清HA含量和肝组织HyP含量，明显增高血清TP和ALB含量，同时可减轻实验鼠肝组织病理改变的程度。结论：APS对CCL4所致实验性慢性肝损伤具有明显的保护作用。     

4种黄酮类化合物对CCl4致小鼠肝纤维化的防治作用

目的探讨芹菜素、根皮苷、原花青素和新橙皮苷二氢查尔酮等黄酮类化合物在CCl4诱导的小鼠肝纤维化模型中的抗肝纤维化作用。方法将♂昆明种小鼠105只随机均分为正常对照组、CCl4模型组、秋水仙碱组、芹菜素组、根皮苷组、原花青素组、新橙皮苷二氢查尔酮组。给药5周后采血并处死小鼠,测定并比较各组小鼠血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)的活性,总蛋白(TP)、白蛋白(ALB)及肝组织中的羟辅氨酸(HYP)的含量,计算小鼠的肝指数,观察肝脏的病理变化。结果 4种黄酮类化合物均可使模型小鼠血清中ALT、AST的含量、肝组织中羟脯氨酸的含量降低;病检也证明各组小鼠的肝细胞变性、坏死和肝纤维化均有不同程度的减轻。结论芹菜素、根皮苷、原花青素及新橙皮苷二氢查尔酮有抗CCl4致小鼠肝纤维化的作用。     

赤芍水提物对四氯化碳致肝损伤大鼠的保护作用

目的：探讨赤芍水提取物对四氯化碳(CCl4)中毒性肝纤维化大鼠的治疗作用。方法：复制大鼠CCl4肝纤维化模型，以马洛替酯为阳性对照，采用光镜观察组织学改变， 测定血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、一氧化氮(NO)、透明质酸(HA)、层粘蛋白(LN)，肝组织羟脯氨酸(Hyp)、丙二醛(MDA)以反映肝细胞损伤及肝纤维化的程度。结果：赤芍水提物能降低实验性肝纤维化大鼠血清中升高的ALT、AST、NO、HA、LN水平和肝组织中过高的Hyp、MDA的含量。病理组织学检查亦表明，赤芍水提物明显改善实验性肝纤维化。结论：赤芍水提物对实验性肝纤维化具有治疗作用。     

四氯化碳对大鼠肝毒性的时量关系研究

目的：探讨四氯化碳随用药时间和剂量的变化对大鼠肝脏功能与组织形态学的损害的时量关系，进一步了解四氯化碳对肝脏的毒理学作用。为研究护肝药提供动物实验模型，方法：大鼠皮下注射60％四氯化碳花生油，每周2次，分别在实验1、3、5、7、9wk观察大鼠血清丙氨酸氨基转移酶（ALT／GPT）、天冬氨酸氨基转氨酶（AST／GOT）、总蛋白（TP）和白蛋白（Alb)，血清透明质酸及肝组织病理变化和内脏器官重量指数的改变，以判断肝脏受损程度。结果：四氯化碳对大鼠肝脏的影响表现在1wk内可致大鼠血清ALT升高，3wk时发生肝组织脂变，5wk时肝组织轻度纤维增生，7wk时肝组织呈纤维化改变，9wk时肝组织发生明显的肝纤维化，甚至肝硬化。结果：大鼠皮下注射60％四氯化碳随染毒时间延长，染毒剂量的增加，对肝脏的毒性也不断加重。     

四氯化碳致大鼠肝纤维化及红苓肝宝的防治作用

目的：研究红苓肝宝对大鼠肝纤维化的防治作用，方法：运用皮下多次注射四氯化碳致大鼠慢性损伤性肝纤维化模型，观察红苓肝宝对大鼠肝组织病理变化。血清透明质酸，血清丙氨酸氨基转移酶（ALT／GPT），天冬氨酸氨基转氨酶（AST／GOT），总蛋白（TP）和白蛋白（Alb)以及内脏器官重量的影响，并与秋水仙碱进行了比较。结果：红苓肝宝在该剂量下大鼠肝纤维化率为45％，而模型组与秋水仙碱肝纤维化率分别为100％和50％，对肝损伤的其他指标观察表明，红苓肝宝对肝损伤的其他指标均有降低作用，与模型组比较，P＜0．01，结论：红苓肝宝在该剂量下对大鼠有明显的抗肝纤维化作用。     

肝心康胶囊对小鼠肝损伤的保护作用

目的 观察肝心康胶囊(GXK)对小鼠3种肝损伤模型的保护作用：方法采用四氯化碳(CCl4)、对乙酰氨基酚(APAP)、D-氨基半乳糖 脂多糖(D-GalN LPS)致小鼠肝损伤的3种模型，测定用药前后血清谷丙转氨酶(ALT)。结果GXK能明显降低CCl4,APAP,D-GalN LPS引起的肝损伤后小鼠血清中升高的ALT水平。结论GXK对实验性肝损伤有明显的保护作用。     

Nachweis einiger Heilmittel in der Kniegelenksynovialflüssigkeit

Zusammenfassung Mittels Gaschromatographie und Dünschichtchromatographie wiesen die Autoren 11 Substanzen nach, welche durch Injektion oder nach Verabreichung per os in die Kniegelenksynovialflüssigkeit eindrangen. In ihrer Aufstellung konnten sie eine direkte Beziehung zwischen Struktur sowie chemischphysikalischen Eigenschaften der Substanz und ihrer Fähigkeit, aus dem Blut in die Kniegelenksynovialflüssigkeit einzudringen, nicht nachweisen, außer der Tatsache, daß Substanzen mit starker Affinität zu Eiweißstoffen erst in höheren Dosen nachweisbar waren.     

Synthesis,Cytotoxicity and Antileishmanial Activity of Some N-(2-(indol-3-yl)ethyl)-7-chloroquinolin-4-amines

We report herein the condensation of 4,7-dichloroquinoline (1) with tryptamine (2) and D-tryptophan methyl ester (3) . Hydrolysis of the methyl ester adduct (5) yielded the free acid (6) . The compounds were evaluated in vitro for activity against four different species of Leishmania promastigote forms and for cytotoxic activity against Kb and Vero cells. Compound (5) showed good activity against the Leishmania species tested, while all three compounds displayed moderate activity in both Kb and Vero cells.     

Emerging drugs for epilepsy

Epilepsy affects ≤ 1% of the world's population. Antiepileptic drugs (AEDs) are the mainstay of treatment, although more than a third of patients are not rendered seizure free with existing medications. Uncontrolled epilepsy is associated with increased mortality and physical injuries, and a range of psychosocial morbidities, posing a substantial economic burden on individuals and society. Limitations of the present AEDs include suboptimal efficacy and their association with a host of adverse reactions. Continued efforts are being made in drug development to overcome these shortcomings employing a range of strategies, including modification of the structure of existing drugs, targeting novel molecular substrates and non-mechanism-based drug screening of compounds in traditional and newer animal models. This article reviews the need for new treatments and discusses some of the emerging compounds that have entered clinical development. The ultimate goal is to develop novel agents that can prevent the occurrence of seizures and the progression of epilepsy in at risk individuals.     

盐酸达泊西汀中甲磺酸甲酯、甲磺酸乙酯及甲磺酸异丙酯的顶空毛细管GC-ECD法测定

建立了衍生化顶空毛细管气相色谱-电子捕获检测器(ECD)法测定盐酸达泊西汀中的甲磺酸甲酯(MMS)、甲磺酸乙酯(EMS)和甲磺酸异丙酯(IMS).应用碘化钠衍生技术,使用PW-5毛细管柱,载气为氮气,ECD检测,程序升温.MMS、EMS和IMS分别在0.03～0.30、0.05～0.50和0.05～0.50 μg/ml浓度范围内线性关系良好,平均回收率分别为63.5％、100.3％和96.2％,最低检测限分别为0.30、0.50和0.50 ng/ml.     

Lung disease and PKCs

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.