植物多糖在胃肠道及肝病中的新作用(英文)

Ｔｈｅｐｏｌｙｓａｃｃｈａｒｉｄｅｆｒａｃｔｉｏｎｆｒｏｍｖａｒｉｏｕｓｈｅｒｂａｌｍｅｄｉｃｉｎｅｓｈａｓｂｅｅｎｗｅｌｌｓｔｕｄｉｅｄｆｏｒｉｔｓｉｍｍｕｎｏｍｏｄｕｌａｔｏｒｙａｃｔｉｏｎａｎｄａｎｔｉｔｕｍｏｒｅｆｆｅｃｔ,ｓｕｃｈａｓｌｅｎｔｉｎａｎａｎｄｌｕｃｉｄＧａｎｏｄｅｒｍａ ,ｆｏｒｍｏｒｅｔｈａｎｔｗｅｎｔｙｙｅａｒｓ .Ｔｈｅｓｅａｃｔｉｏｎｓａｎｄｅｆｆｅｃｔｓｍａｙｂｅｄｕｅｔｏｓｔｉｍｕｌａｔｉｏｎｏｆｔｈｅｐｈａｇｏｃｙｔｉｃａｃｔｉｖｉｔｙａｎｄａｎｔｉ ｉｎｆｌａｍ…     

植物及真菌多糖抗白血病作用

白血病是造血系统的恶性肿瘤，迄今为止由于化疗和放疗都具有一定的毒副作用而制约了其应用。多糖由于其无明显的毒副作用，且其代谢产物可以成为人体的营养物质，而无有毒代谢物的蓄积，因此，自上世纪50年代末发现真菌多糖的抗肿瘤作用以来，学者们对植物多糖与真菌多糖在治疗白血病方面的作用作了大量的研究。     

植物多糖的抗肿瘤作用研究

近年来,有关多糖类的研究进展迅速,中药多糖的抗肿瘤作用已得到人们的肯定.具有抗肿瘤活性的中药多糖主要来自动物多糖、植物多糖和微生物多糖 3个方面.其中,植物多糖因具有多种生物活性而备受人们关注,包括枸杞多糖、人参多糖、黄芪多糖、芦荟多糖等.     

香菇多糖在肝病治疗中的配伍应用

香菇多糖是一种免疫增强,它具有保护肝脏的作用等[1]。因此,临床上广泛应用于肝炎、肝硬化和肝癌等肝病的治疗,具有提高疗效、减少不良反应等优点。现在将香菇多糖的配伍用药归纳起来,供广大医务工作者参考。     

南五味子多糖急性毒性及对小鼠肝损伤保护作用的研究

摘 要 目的：研究南五味子多糖的急性毒性及对四氯化碳（CCl4）致小鼠肝损伤的保护作用。方法: 采用经典的急性毒性实验方法,测定南五味子多糖的最大给药量（MLD）,并观察其急性毒性反应;采用0.5% CCl4致小鼠急性肝损伤模型,将60只小鼠随机分为空白对照组、CCl4模型对照组、联苯双酯组及南五味子多糖高（1 388 mg·kg^-1）、中（694 mg·kg^-1）、低（347 mg·kg^-1）剂量组,每组10只,连续给药6 d,检测血清中AST和ALT水平,观察肝脏的损伤程度。结果: 急性毒性实验中对小鼠的一般行为、体质量变化及各脏器检查均未见异常,南五味子多糖毒性症状不显著;与模型对照组比较,南五味子多糖3个剂量组的ALT水平显著降低（P<0.05或P<0.01）,南五味子多糖高、中剂量组的AST水平显著降低（P<0.01）,一定程度上改善了肝脏组织损伤。结论:南五味子多糖无显著毒性,对CCl4致小鼠急性肝损伤具有一定的保护作用。     

植物中的生物活性多糖

评述了1977年1月至1988年12月间从自然界分离出的生物活性多糖。除生物活性外,还讨论了用于它们的分离,纯化和结构测定的现代技术。     

蛴螬多糖的急性毒性及对肝损伤的保护作用

目的评价蛴螬多糖的急性毒性并研究其对肝损伤的保护作用。方法用最大耐受量法测定蛴螬多糖小鼠腹腔注射的急性毒性。高剂量重复给药2周,观察肝功能及病理改变。采用四氯化碳(CCl_4)建立小鼠急性肝损伤模型,通过检测血清酶水平及肝组织病理改变来评价蛴螬多糖对急性肝损伤的影响。体外培养正常人肝细胞HL7702,MTT法测定蛴螬多糖对肝细胞活力的影响,丙二醛(MDA)和超氧化物歧化酶(SOD)含量测定分别检测蛴螬多糖对脂质过氧化的影响。结果蛴螬多糖对小鼠腹腔注射的最大耐受量为8 g·kg~(-1)。高剂量重复给药2周可明显降低正常大鼠肝脏中谷草转氨酶(AST)的含量,但对肝组织结构和凝血时间等无明显影响。蛴螬多糖25,50和100 mg·kg~(-1) 3个剂量组均可降低模型血清谷丙转氨酶(ALT)、AST和碱性磷酸酶(ALP)的水平,减轻肝损伤的组织病理变化程度;且呈剂量依赖性。体外实验发现,蛴螬多糖质量浓度在0.1～100 mg·L~(-1)范围内对肝细胞无毒,质量浓度为0.3～100 mg·L~(-1)时可抑制受损肝细胞,存活率下降;蛴螬多糖能明显抑制受损肝细胞MDA水平的升高和SOD活性的减弱。结论蛴螬多糖腹腔注射无明显毒性,大剂量注射未引起肝损伤;对CCl_4诱导的小鼠急性肝损伤具有明显的保护作用,其机制可能与抗氧化有关。     

绞股蓝多糖对小鼠四氯化碳肝损伤的保护作用

目的从绞股蓝中分离纯化绞股蓝多糖,并研究绞股蓝多糖对小鼠CCl4肝损伤的保护作用。方法经去蛋白、除果胶、脱色、超滤之后得绞股蓝多糖,以绞股蓝多糖对小鼠连续灌胃7 d之后,腹腔注射0.5%的CCl4花生油溶液,建立肝损伤模型,继续给药2次,检测血清丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)活性;测定肝组织中丙二醛(MDA)含量和谷胱甘肽(GSH)活性;采用光学显微镜观察肝组织病理组织学变化。结果绞股蓝多糖各剂量组能明显抑制肝损伤小鼠ALT、AST活性的升高;抑制肝组织中MDA含量的升高,提高肝组织中GSH活性;减轻CCl4对肝脏细胞的病理损伤。结论绞股蓝多糖对CCl4造成的小鼠急性肝损伤具有明显保护作用。     

云芝多糖对小鼠免疫性肝损伤的保护作用

目的：探讨云芝多糖（CVP）对免疫性肝损伤的保护作用及其机制。方法：昆明种小鼠随机分为5组,分正常对照组;病理造模组;CVP保护组分高、中、低三组。造模第一天,除正常对照组外,其余各组小鼠经尾静脉注射2．5mg卡介苗（BCG）;CVP低、中、高保护组每天分别按体重100mg／kg、200mg/kg、300mg／ksCVP灌胃1次,正常对照组和模型组用生理盐水同样处理,第十二天用CVP灌胃给药2h后,模型组和CVP各保护组从尾静脉注射7．5μg,只脂多糖（LPS）;16h后称取小鼠体重,眼球取血分离血清测定丙氨酸转氨酶（ALT）;处死小鼠立即取出肝脏、胸腺称重,计算肝体指数和胸腺指数,制备肝匀浆测定丙二醛（MDA）,取相同部位的肝组织,制作病理切片,HE染色,光镜下观察肝组织损伤程度。结果：与模型组比较,CVP各保护组均可降低免疫性肝损伤小鼠肝体指数,增加胸腺指数;降低小鼠血清中ALT的活性和和肝匀浆中MDA的含量,减轻肝细胞气球样变性,点状、片状坏死及炎性细胞浸润。结论：CVP对小鼠免疫性肝损伤有保护作用。     

联合测定胃病患者血浆及胃窦粘膜胃泌素生长抑素的意义研究

用ＲＩＡ法同时测定了１３例轻度浅表性胃炎（ＣＳＧ）、２５例胃溃疡（ＧＵ）及１２例胃癌（ＧＣ）患者血浆及胃窦粘膜胃泌素（Ｇａｓ）和生长抑素的含量。结果表明：血浆Ｇａｓ在ＧＵ组显著高于ＣＳＧ组（Ｐ＜０．０５）；胃窦粘膜Ｇａｓ则呈现ＧＣ组＞ＧＵ组＞ＣＳＧ组的趋势，但仅在ＧＣ与ＣＳＧ组间有统计学差异。血浆ＳＳ（ｓｏｍａｔｏｓｔａｔｉｎ生长抑素）的含量变化为ＧＣ组＜ＧＵ组＜ＣＳＧ组，各组间差别均有显著性；而胃窦粘膜ＳＳ水平则在ＧＣ组显著高于其余各组，ＧＵ组低于ＣＳＧ组。在ＣＳＧ和ＧＵ患者Ｇａｓ、ＳＳ的血浆与胃窦粘膜含量间均呈正相关，而在ＧＣ组仅见粘膜Ｇａｓ与ＳＳ间呈正相关。提示：血浆和胃窦粘膜Ｇａｓ和ＳＳ的变化可能在胃病发病机制中起重要作用，联合检测血浆及胃窦粘膜ＳＳ可能有助于胃癌的早期诊断。     

CALCITONIN GENE RELATED PEPTIDE: VASODILATOR IN OVINE HEPATIC AND RENAL VASCULATURE

1. Calcitonin gene-related peptide (CGRP) is a product of alternate splicing of the calcitonin gene. It is found in nerves in the vasculature and is known from in vitro studies to be a potent vasodilator. It is found abnormally in the circulation of patients with medullary thyroid carcinoma (MTC) and has been proposed to be a cause of symptoms. This study was designed to determine the dose-response effects of CGRP infusion in the intact conscious sheep on blood flow to liver and kidney, organs known to be richly innervated by CGRP-containing nerves. 2. Blood flow was measured by an indicator dilution technique using [131I]-labelled iodohippurate. CGRP infusion at both 1 and 5 pmol/kg per min produced significant (P less than 0.05) increases in both renal and hepatic blood flow. This increase in flow occurred despite a significant fall in perfusion pressure (P less than 0.05) at the higher infusion rate. At the highest infusion rate of 10 pmol/kg per min, when fall in perfusion pressure was even more marked, renal and hepatic blood flow was maintained. 3. We conclude that CGRP is vasodilatory in the renal and hepatic vascular beds and propose that nerves containing CGRP in those vessels may have a role in maintaining blood flow to those organs.     

BUPRENORPHINE AND GASTROINTESTINAL TRANSIT IN RATS: EFFECT OF NALOXONE ON THE BIPHASIC DOSE-RESPONSE CURVE

1. Buprenorphine (0.01-10 mg/kg, subcutaneous [s.c.]) slowed the passage of a charcoal meal along the gastrointestinal tract in rats. The dose-response relationship was U-shaped. 2. When rats were pretreated with naloxone (0.30 mg/kg, s.c.), both the descending and ascending components of the buprenorphine dose-response curve were displaced to the right. 3. Buprenorphine-induced delay of transit was maximal at a dose of 0.10 mg/kg. In rats pretreated with naloxone, a 30-fold higher dose of buprenorphine was required for a comparable peak effect. 4. Moderate-high doses of buprenorphine may be acting on a functionally related binding site which non-competitively inhibits the usual buprenorphine-mu opioid receptor interaction.     

THE HEPATIC TRANSPORT OF TAUROCHOLIC ACID IN THE RAT: DEVELOPMENT OF A MATHEMATICAL MODEL

1. The transport of taurocholic acid from portal blood to bile was studied in the anaesthetized rat by injecting a radiolabeled pulse of bile acid. 2. The transport process was very rapid, 50% of the dose being secreted within 5 min, and the total dose within 15 min. 3. The transport process had a large capacity. The secretory profile was little modified by a 500-fold increase in the injected dose. 4. The transport process was modelled with both analogue and digital computers. The simplest model which fitted the data comprised rapid uptake from portal blood, slow transport across the cell and rapid secretion into bile. The digital computer simulation suggested that this model is not unique, but will require further testing.     

DISTRIBUTION OF CADMIUM IN BODY ORGANS AND HEPATIC METALLOTHIONEIN CONTENT FOLLOWING CHELATION THERAPY

1. Calcium trisodium diethylene triamine penta-acetate (CaNa3DTPA), sodium 1,2 diaminocyclohexane tetra-acetate (Na2CDTA), triethylenetetramine hydrochloride (TETA.HCl) and sodium diethyldithiocarbamate (NaDDC) were investigated for their efficacy to mobilize cadmium (Cd) from various tissues and hepatic metallothionein (MT) in Cd-exposed rats. 2. All chelating agents reduced the hepatic Cd burden but did not elicit any influence on other tissues, except that TETA.HCl lowered pancreas Cd and NaDDC increased brain Cd. 3. Cadmium-induced hepatic MT was lowered upon treatment with CaNa3DTPA while it increased further following treatment with NaDDC. 4. The chelating agents, in split doses, are capable of reducing the hepatic burden of Cd and altering the hepatic MT level. 5. While all the chelating agents decreased Cu content of hepatic MT, only CaNa3DTPA decreased its Zn content and TETA.HCl mobilized MT-bound Cd. 6. The administration of chelating agents alone in normal animals showed that NaDDC induced greater hepatic MT synthesis and increased MT-bound Zn than other chelating agents.     

ROLE OF HEPATIC FATTY ACID:COENZYME A LIGASES IN THE METABOLISM OF XENOBIOTIC CARBOXYLIC ACIDS

1. Formation of acyl-coenzymes (Co)A occurs as an obligatory step in the metabolism of a variety of endogenous substrates, including fatty acids. The reaction is catalysed by ATP-dependent acid:CoA ligases (EC 6.2.1.1-2.1.3; AMP forming), classified on the basis of their ability to conjugate saturated fatty acids of differing chain lengths, short (C₂-C₄), medium (C₄-C₁₂) and long (C₁₀-C₂₂). The enzymes are located in various cell compartments (cytosol, smooth endoplasmic reticulum, mitochondria and peroxisomes) and exhibit wide tissue distribution, with highest activity associated with liver and adipose tissue. 2. Formation of acyl-CoA is not unique to endogenous substrates, but also occurs as an obligatory step in the metabolism of some xenobiotic carboxylic acids. The mitochondrial medium-chain CoA ligase is principally associated with metabolism via amino acid conjugation and activates substrates such as benzoic and salicylic acids. Although amino acid conjugation was previously considered an a priori route of metabolism for xenobiotic-CoA, it is now recognized that these highly reactive and potentially toxic intermediates function as alternative substrates in pathways of intermediary metabolism, particularly those associated with lipid biosyntheses. 3. In addition to a role in fatty acid metabolism, the hepatic microsomal and peroxisomal long-chain-CoA-ligases have been implicated in the formation of the acyl-CoA thioesters of a variety of hypolipidaemic and peroxisome proliferating agents (e.g. cloflbric acid) and of the r (-)-enantiomers of the commonly used 2-arylpropionic acid non-steroidal anti-inflammatory drugs (e.g. ibuprofen). In vitro kinetic studies using rat hepatic microsomes and peroxisomes have alluded to the possibility of xenobiotic-CoA ligase multiplicity. Although cDNA encoding a long-chain ligase have been isolated from rat and human liver, there is currently no molecular evidence of multiple isoforms. The gene has been localized to chromosome 4 and homology searches have revealed a significant similarity with enzymes of the luciferase family. 4. Increasing recognition that formation of a CoA conjugate increases chemical reactivity of xenobiotic carboxylic acids has led to an awareness that the relative activity, substrate specificity and intracellular location of the xenobiotic-CoA ligases may explain differences in toxicity. 5. Continued characterization of the human xenobiotic-CoA ligases in terms of substrate/inhibitor profiles and regulation, will allow a greater understanding of the role of these enzymes in the metabolism of carboxylic acids.     

EFFECTS OF ADRENALINE AND ISOPRENALINE ON HEPATIC VENOUS HAEMODYNAMICS AND VENOUS RETURN IN THE DOG

1. The effects of adrenoceptor agonists on venous haemodynamics were examined, utilizing the lower half perfusion method in dogs. 2. Femoral arterial pressure, central venous pressure, thoracic vena caval flow, abdominal vena caval flow, renal venous flow and femoral venous flow were measured simultaneously using electronic transducers and electromagnetic flow-meters. Hepatic volume change was monitored by the strain-gauge arch. 3. Single injections of both adrenaline (1.0 μ/kg) and isoprenaline (1.0 μg/kg) intra-aortically produced an increase in venous return, adrenaline transiently and isoprenaline continuously. 4. Epinephrine increased hepatic venous flow, while isoprenaline increased only abdominal vena caval flow. 5. These findings suggest that effects of α-adrenoceptors are more pronounced on the hepatic vein, while on other peripheral veins, effects of β-adrenoceptors are more pronounced.     

A COMPARISON OF THE EFFECTS OF END-TO-SIDE PORTACAVAL SHUNTING AND SIDE-TO-SIDE MESOCAVAL SHUNTING ON HEPATIC HAEMODYNAMICS IN THE DOG

Functional liver blood flow and hepatic artery flow were measured before and after either end-to-side portacaval or side-to-side mesocaval shunting in dogs. Functional liver blood fell by approximately 50% following both portacaval and mesocaval shunting. The hepatic artery response was variable after both portacaval and mesocaval shunts. It is concluded that side-to-side mesocaval shunts do not preserve hepatic blood flow or produce a greater compensatory increase in hepatic artery flow than conventional portacaval shunts.     

肝动脉栓塞微球的动物体内行为和药效学研究

肝动脉栓塞微球是用于治疗中晚期肝癌的新剂型。通过动脉插管即可将微球栓塞至肝癌邻近的末梢动脉血管,起阻断血流和在局部缓释药物的双重作用。本文结合几年来对MTX明胶微球和顺铂-乙基纤维素微球的基础研究工作,综述微球栓塞后在动物体内的行为和药效学,并介绍了初期临床结果。     

HEPATIC SINUSOIDAL RESPONSES TO INTRAPORTAL INJECTIONS OF PHENYLEPHRINE AND ISOPRENALINE IN THE RAT

1. Specific α- and β-adrenoreceptor agonists, phenylephrine and isoprenaline, were injected intraportally into the intact rat liver under direct microscopic observation by an in viva transillumination technique. 2. The diameter of a hepatic sinusoid and the intra-sinusoidal erythrocyte velocity were quantitatively measured, and the sinusoidal volume flow was calculated from these two parameters. 3. Results show that phenylephrine causes a sinusoidal constriction and an increased sinusoidal blood flow, whereas isoprenaline causes the opposite effects on the sinusoids. 4. All the sinusoidal responses to phenylephrine and isoprenaline were dose-dependent and were possibly related to the direct effect of these drugs on the sinusoids.