不同给药途径的姬松茸多糖对鼠急性肝损伤的保护效应及其抗氧化作用的研究

分别通过灌胃、皮下注射的方法，给予小鼠姬松茸多糖灭菌溶液．连续7d。然后经四氯化碳染毒12h岳．采血并制备肝组织匀浆液进行GPT、GOT活性及SOD、MDA含量的检测。结果表明：用姬松茸多糖灌胃比皮下注射能更快、更有效的保护肝损伤；而SOD活性及HDA含量未见有统计学差异。     

姬松茸水溶性粗多糖对小鼠镉中毒治疗作用研究

目的:探讨姬松茸水溶性粗多糖对镉中毒小鼠治疗作用。方法:将40只SPF级雄性健康小白鼠随机分为对照组、模型组、多糖治疗组。造模5周后,多糖治疗组用300 mg/kg.d多糖治疗20d。结果:与对照组比较,模型组小鼠肝脏指数、肾脏指数、ALT、AST、MDA含量显著升高(P0.05),TP、GSH、GSH-Px含量显著降低(P0.05)。与模型组比较,多糖治疗组小鼠的肝脏指数、肾脏指数、ALT、AST和MDA含量显著降低(P0.05),TP、GSH、GSH-Px含量显著升高(P0.05)。表明灌胃姬松茸水溶性粗多糖溶液对小鼠镉中毒有一定的治疗作用。     

姬松茸多糖对小鼠急性肝损伤的保护作用及其霉性反应的研究

为了研究姬松茸多糖对小鼠急性肝损伤的保护作用及其毒性反应,我们设计了两个试验方案:第一,先用四氯化碳(CCl4)攻毒后立即注射姬松茸多糖;第二,给小鼠注射不同高剂量的姬松茸多糖后在攻毒。结果表明:攻毒组GPT活性显著高于对照组,证实姬松茸多糖具有护肝作用;一定剂量范围内的姬松茸多糖未见有毒性反应,且对肝脏的保护呈现良好的量效关系。     

姬松茸及其多糖的研究进展

姬松茸是一种食药兼用的名贵真菌,具有营养保健作用。姬松茸多糖具有抗肿瘤、抗氧化、提高动物机体免疫力等功效。介绍了姬松茸所含的功能性物质及姬松茸多糖的功能,并就姬松茸及其多糖的研究进展进行了展望。     

姬松茸多糖对小鼠急性肝损伤的保护作用及其毒性反应的影响

为了研究姬松茸多糖对小鼠急性肝损伤的保护作用及其毒性反应，我们设计了两个试验方案：第一，先用四氯化碳(CCl4)攻毒后立即注射姬松茸多糖；第二，给小鼠注射不同高剂量的姬松茸多糖后在攻毒。结果表明：攻毒组GPT活性显著高于对照组，证实姬松茸多糖具有护肝作用；一定剂量范围内的姬松茸多糖未见有毒性反应，且对肝脏的保护呈现良好的量效关系。     

姬松茸多糖对AA肉鸡免疫功能的影响

姬松茸不但是一种美味的食用真菌,而且具有重要的药用作用一姬松茸含有多种生物活性物质,具有抑制肿瘤生长、降血脂、改善动脉硬化、防治糖尿病和增强人体免疫力等功效近年来,人们对姬松茸提取物特别是姬松茸多糖免疫活性的研究越来越感兴趣:研究表明,姬松茸多糖能够促进免疫器官的增殖,增强机体的非特异性免疫、体液免疫和细胞免疫,促进超敏反应的发生.Nakajima等(2002)研究发现姬松茸子实体沸水提取物可以刺激小鼠T细胞和巨噬细胞分泌白细胞介素-1 β (Interleukin-1β,IL-1 β)和IL-6,且能刺激小鼠产生大量的抗体.刘常金等(2002)研究了姬松茸多糖的免疫调节作用,研究发现,姬松茸多糖可促进免疫器官的增殖,延缓其衰退,促进迟发型超敏反应(DTH)的发生,能增强巨噬细胞的吞噬功能,但对体液免疫的作用不明显.张卉等(2007)研究了姬松茸胞外多糖AbEXPI-a免疫调节活性,研究发现此多糖可以全面提高小鼠的免疫功能,对非特异性免疫、体液免疫和细胞免疫均具有促进作用.可见,在不同的实验研究中姬松茸多糖的功能并不一致.     

灵芝活性组分在小鼠体内的降糖功效研究

为了探究灵芝活性组分灵芝多肽、多糖的降血糖机理,采用四氧嘧啶建立糖尿病小鼠模型,经不同组分灵芝提取物灌胃连续4周后测定空腹血糖值、胰岛素浓度、肝糖原、肌糖原含量、肝脏SOD活性MDA含量。结果表明,灵芝多糖能有效增加小鼠血清胰岛素浓度(P0.05);灵芝多肽和多糖可显著降低糖尿病小鼠空腹血糖含量,降糖率分别为19.1%和29.8%;显著增强小鼠肝脏SOD活性(P0.05),升高率分别为13.4%和19.7%;降低肝脏MDA含量(P0.05),且分别降低了27.8%和35.1%。     

茯苓多糖对糖尿病小鼠淋巴细胞DNA损伤及肾组织主要抗氧化酶活性的影响

为研究茯苓多糖对2型糖尿病(NIDDM)小鼠淋巴细胞DNA损伤及肾组织主要抗氧化酶活性的影响,试验采用高糖高脂饲料+小剂量链脲佐菌素(STZ)方式诱导NIDDM动物模型,然后将动物分成正常对照组、模型对照组、茯苓多糖灌胃组、罗格列酮灌胃组,药物连续灌胃42 d后,检测小鼠淋巴细胞DNA损伤,肾组织超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性以及丙二醛(MDA)含量。结果表明:WRP对NIDDM小鼠淋巴细胞DNA损伤具有修复作用,能提高糖尿病小鼠肾组织中SOD、GSH-Px、CAT活性,降低MDA的含量。表明茯苓多糖能增强肾脏抗氧化性,保护自由基介导的氧化损伤,可以治疗或延缓糖尿病肾病(DN)的发生。     

姬松茸多糖对雏鸡体内抗细菌感染作用的研究

为了研究姬松茸多糖对雏鸡体内抗细菌感染的作用,试验分为7组,即姬松茸多糖低浓度大肠杆菌试验组(1组)、姬松茸多糖高浓度大肠杆菌试验组(2组)、大肠杆菌对照组(3组)、空白对照组(4组)、姬松茸多糖低浓度巴氏杆菌试验组(5组)、姬松茸多糖高浓度巴氏杆菌试验组(6组)、巴氏杆菌对照组(7组)。1,2,5,6组雏鸡分别灌服低剂量或高剂量的姬松茸多糖,3,4,7组雏鸡分别灌服等量的生理盐水,连续用药14 d,之后除4组外,各组雏鸡分别感染大肠杆菌或巴氏杆菌,观察各组雏鸡的临床症状并记录体重变化。第28天后剖检,测定免疫器官指数,进而研究姬松茸多糖对雏鸡抗细菌感染的效果。结果表明:经细菌感染后,口服高剂量姬松茸多糖组与其他各组相比,雏鸡体重和免疫器官指数变化差异明显。说明口服高浓度姬松茸多糖能够促进家禽免疫器官的发育,进而提高机体的免疫力,对抗细菌感染,可应用到畜牧生产和兽医临床应用中。     

磷酸化姬松茸多糖对小鼠的抗感染作用研究

为了研究磷酸化姬松茸多糖对小鼠的抗感染作用,试验对小鼠经口灌服磷酸化姬松茸多糖14 d,同时设立姬松茸多糖对照组和空白对照组,各组小鼠均在试验第15天和第29天经口感染大肠杆菌,记录各组小鼠的体重、感染第29天和第36天的脾脏指数,并检测血清中抗大肠杆菌Ig G效价。结果表明:磷酸化姬松茸多糖能够促进和维持脾脏的发育,提高机体的体液免疫应答,进而对抗细菌感染,而且磷酸化姬松茸多糖的免疫调节作用和抗感染作用均好于姬松茸多糖,可用于兽医临床治疗以及疾病预防和控制。     

中药复合剂AFF-Ⅰ口服液对小鼠急性肝损伤血液生化指标的影响

为了研究中药复合剂AFF-Ⅰ口服液对四氯化碳(CCl4)导致小鼠急性肝损伤的保护效果,将60只昆明种小鼠随机分为正常对照、造模、阳性药物对照(联苯双酯)、中药复合剂AFF-Ⅰ口服液高、中、低剂量6组。正常对照组、造模组分别灌服等量的生理盐水,阳性药物对照组按150mg/kg灌胃联苯双酯溶液,中药复合剂AFF-Ⅰ口服液高、中、低剂量组分别按45、30、15mL/kg灌胃,2次/d,连续给药7d。末次给药后1h,正常对照组腹腔注射花生油20mL/kg,其余组腹腔注射10mL/L CCl4花生油溶液20mL/kg,16h后测定血清中天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)含量和肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)含量。结果表明,中药复合剂AFF-Ⅰ口服液低、中、高剂量组能显著降低CCl4导致小鼠急性肝损伤血清中AST、ALT含量(P<0.01),显著降低CCl4所致急性肝损伤小鼠肝组织MDA含量,提高肝组织SOD活力(P<0.01)。研究表明,中药复合剂AFF-Ⅰ口服液对小鼠的急性肝损伤具有保护作用。     

脱落酸对四氯化碳致小鼠急性肝损伤的保护作用

研究脱落酸(ABA)对四氯化碳所致小鼠急性肝损伤的保护作用。70只ICR小鼠随机分为空白组、空白对照组、模型组、联苯双酯组、ABA高、中、低剂量组,连续ig给药10 d,于末次给药1 h后,除空白组和空白对照组按0.01 m L/g注射橄榄油外,其余各组均按体重注射体分数10%的CCl_4(CCl_4用橄榄油稀释),6 h后,脊椎脱臼处死小鼠,收集血液,检测血清中ALT、AST、TC、TG、HDL-c水平,取肝脏制备肝匀浆测定GSH-Px、MDA、SOD活性,HE染色,光镜下观察肝组织病理变化。结果表明:ABA各剂量组均能明显改善因CCl_4造成肝损伤引起的血脂异常,一定剂量的ABA可以降低肝损伤小鼠血清中ALT、AST水平的升高,降低肝匀浆中小鼠MDA含量,升高SOD、GSH-Px活性,减轻CCl_4对肝组织的病理损伤。ABA对CCl_4致小鼠急性肝损伤具有一定的保护作用,其保护机制可能与改善小鼠因CCl_4致小鼠急性肝损伤引起的血脂异常,清除自由基,抑制脂质过氧化,减轻肝组织的损伤有关。     

龙葵对四氯化碳致小鼠急性肝损伤的保护作用

研究了龙葵对四氯化碳（CCl4）所致小鼠急性肝损伤的保护作用。将60只小鼠随机分成6组：正常对照组、模型组、龙葵高剂量组、龙葵中剂量组、龙葵低剂量组、阳性对照组（水飞蓟素）。给药7 d后除正常组外其余5组按10 mL/kg剂量给予0.35% CCl4 。分别检测血清中丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）和肝功能氧化指标：丙二醛（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）。通过统计学处理分析得出龙葵各剂量组与阳性对照组、正常组和模型组之间存在差异性。结果表明,通过龙葵高剂量组的保护作用可以使血清中ALT、AST活性和肝组织中的MDA含量、SOD和GSH-Px活力趋近于正常水平。证明龙葵对CCl4所致小鼠急性肝损伤有明显的保护作用。     

芽孢杆菌发酵五味子提取液对肉鸡肝损伤的影响

为探索中药与益生菌联用治疗肉鸡肝损伤的新方法,从而改善畜禽＂亚健康＂,本研究以CCl4注射肉鸡,建立肝损伤模型,并利用芽孢杆菌发酵五味子提取液,将发酵提取液混饮肝损伤肉鸡,检测外周血谷草转氨酶（Aspar-tate transaminase,AST）、谷丙转氨酶（Alanine aminotransferase,ALT）、过氧化物岐化酶（Superoxide dismutase,SOD）、丙二醛（Malondialdehyde,MDA）、谷胱甘肽还原酶（Glutathione reductase,GR）含量,并进行组织病理学观察。结果显示,芽孢杆菌在五味子提取液与培养基1∶1（V/V）混合液中生长良好,五味子有效成分在发酵前后含量无明显变化,发酵提取液按0.5%、1%混饮7d后,与肝损伤阳性对照组相比,2个用药组AST（P〈0.05）、ALT（P〈0.05）、SOD（P〈0.05）、GR（P〈0.01）含量显著升高,MDA（P〈0.05）含量显著降低,肝脏病变较轻。结果表明,芽孢杆菌发酵五味子提取液对提高机体抗氧化能力具有一定的作用,能够治疗肉鸡肝损伤。     

Protective effect of a lignan-containing flaxseed extract against CCl(4)-induced hepatic injury

Carbon tetrachloride (CCl(4)) -induced hepatotoxicity is a commonly used model for investigating lipid peroxidation-related tissue injury. In the present study, the effect of flaxseed extract was observed on histological sections, glutathione-content and DNA strand breaks. Lignan-containing flaxseed extract (1.6 g/kg body weight/day) was daily administered with intragastric injection to rats for three days, on the fourth day, CCl(4) (2 g/kg) was intraperitoneally injected. Liver tissue was sampled at 24 hr after administering CCl(4). Liver-necrosis was observed in CCl(4)-injected rats without pretreatment of flaxseed extract. Pretreatment of flaxseed extract reduced extent of the necrosis found 24 hr after the intraperitoneal administration of CCl(4). Pretreatment of flaxseed extract protect against CCl(4)-induced decrease of reduced glutathione-content measured from reactions with 5,5'-dithiobis-(2-nitrobenzoic acid) and also protect against the elevation of DNA strand breaks in the liver cells measured by comet assay. Flaxseed-extract appears to protect liver cells against CCl(4)-induced necrosis.     

Comparative studies on serum arginase and transaminases in hepatic necrosis in various species of domestic animals

Serum concentrations of arginase, glutamic pyruvic transaminase (SGPT) and glutamic oxaloacetic transaminase (SGOT) in dogs, cats, horses, cattle, sheep and pigs were determined before and after oral administration of CCl(4) at doses known to cause hepatic necrosis. Following CCl(4) administration, serum concentration of arginase and SGOT increased to a level of diagnostic significance in all animals. SGPT increased markedly in dogs and cats and marginally in 1 of 3 cattle and 2 of 3 pigs. In the surviving animals, the serum concentration of arginase returned to normal range much earlier than SGPT or SGOT. Based on the CCl(4) experimental toxicity results of this study, an elevated level of serum arginase would appear to be a reliable indicator of hepatic necrosis in both small and large animals whereas SGPT would be a reliable indicator of hepatic necrosis only in dogs and cats.     

小剂量四氯化碳结合乙醇制备小鼠慢性肝损伤模型

通过腹腔注射70 g/L四氯化碳/橄榄油及自由饮用100 mL/L乙醇建立稳定的小鼠慢性肝损伤模型。选择昆明小鼠25只,试验组15只,对照组10只,试验组腹腔注射70 g/L四氯化碳并自由饮用100mL/L乙醇溶液,连续造模4周。结果试验组小鼠血清中ALT、AST含量明显高于对照组,SOD含量显著低于对照组,病理学切片显示,试验组动物肝脏脂肪细胞增多,并出现少量纤维化。结果表明,小剂量四氯化碳结合乙醇可用于制备小鼠慢性肝损伤模型。     

Effect of vitamin A and/or E on plasma enzymatic antioxidant systems and total antioxidant capacity of broiler chickens challenged with carbon tetrachloride

This study was conducted to investigate the effect of vitamin A and E supplementation on the antioxidant defences of broiler chickens against carbon tetrachloride (CCl(4))-induced oxidative stress at 4 weeks of age. Superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities as well as total antioxidant (TAO) level were analysed before and after CCl(4) challenge. Day-old Lohman broiler chickens (n = 144) were randomly assigned to six factorially arranged dietary treatments consisting of vitamin A [1.35 (control) or +20 mg/kg] and vitamin E [20 (control), +40 or +60 mg/kg]. The background of vitamins A and E in the basal diet was 4500 IU (1.35 mg) and 30 IU (20 mg) respectively. At 4 weeks of age, eight chickens from each treatment were bled before interperitoneal injection with 1 ml of CCl(4) (mixed with olive oil in a ratio of 1:1) and bled again 24 h post-injection. Vitamin E supplementation decreased (p < 0.05) the activity of both SOD and GPX and showed a tendency (p = 0.07) for TAO reduction. CCl(4) attenuated SOD and GPX activities as well as TAO level. The decrease was profound (p < 0.05) in chickens fed the basal diet as well as those fed basal diet supplemented with 20 mg vitamin A. TAO levels behaved similarly when chickens were challenged with CCl(4). After CCl(4) injection, SOD activities of all experimental groups were equivalent. The presence of vitamin A decreased (p < 0.05) plasma GPX activity in chickens fed the basal diet supplemented with 40 mg/kg of vitamin E. Results of this experiment suggested that vitamin E supplementation elevated antioxidant enzyme activities while vitamin A supplementation attenuated this effect. Vitamin E supplementation improved the total reducing power by maintaining comparable levels of TAO upon CCl(4) challenge. Further experiments need to be carried out to investigate the role of vitamin A in oxidative stress and to evaluate the lipid peroxidation products.     

Accumulation of diacylglycerol induced by CCl4-derived radicals in rat liver membrane and its inhibition with radical trapping reagent--FT-IR spectroscopic and HPLC chromatographic observations

We have investigated the accumulation of diacylglycerol (DAG) induced by carbon tetrachloride (CCl4)-derived radicals in the liver of female Sprague-Dawley (SD) rats after intraperitoneally injecting CCl4. DAG is an intracellular activator of protein kinase C (PKC) which regulates cell proliferation and differentiation. The electron spin resonance (ESR) study gave the signal of the PBN-CCl3 adduct in the liver of the rats which were pretreated with PBN, confirming that CCl4 was metabolized into CCl3. radicals with cytochrome P450 enzyme and indicating that PBN could trap them. The blood biochemical assay supported the trapping of the CCl3. radicals; the pretreatment of rats with PBN inhibited the increase in the GOT and GPT values upon exposure to CCl4. The Fourier transform-infrared (FT-IR) study indicated in comparison with the model compounds that the CCl4-injected rats accumulated DAG in addition to phosphatidylcholine, phosphatidylethanolamine and triglyceride (TG) in the lipid membrane fraction of the liver homogenate. DAG was found to be ca. 10-15% of the membrane phospholipids by weight. However, DAG was not found in the lipid of the liver microsomes, suggesting that it is formed only in the cell membrane of liver. Also, neither DAG nor TG was found in the lipid membrane of the rats that were pretreated with PBN followed by an injection of CCl4. The formation of DAG was confirmed by an HPLC study. The activation of PKC was observed in liver homogenate in the rats that were injected with CCl4. On the basis of the above findings, it was concluded that the CCl4-derived radicals stimulate PKC through the accumulation of DAG in the liver membrane of the rats. Furthermore, it was shown that PBN has a protective and therapeutic effect against CCl4-induced damage.     

Reduction of carbon tetrachloride-induced hepatotoxic effects by oral administration of betaine in male Han-Wistar rats: a morphometric histological study

Eighty-five male Han-Wistar rats were arranged into three groups: CCl4-exposed rats, CCl4 + betaine-exposed rats, and control rats. To see the effect of betaine alone, five rats of the control and of the CCl4 + betaine groups were sacrificed after 7 days, before exposure to CCl4. After that, two of the groups (the CCl4 and CCl4 + betaine groups) were exposed to CCl4 (1 ml/kg per day subcutaneously [SC] for 4 consecutive days), and one of the groups (control group) was given olive oil (1 ml/kg per day SC for 4 consecutive days). At the start of the study (day 0), day 1, day 2, day 3, day 4, and 3 days after the last CCl4 and olive oil injections (day 7), samples of five rats per group were sacrificed, and the livers were taken for chemical analyses and histological examination. Oral betaine, after the acclimation period of a week, increased the number of mitochondria but not mitochondria size (day 0), compared with the case in control rats. Exposure to CCl4 resulted in centrilobular hepatic steatosis, and the administration of betaine significantly reduced this. Morphometric analyses also revealed that the addition of betaine increased the volume density of rough endoplasmic reticulum (RER) in the perinuclear areas of liver cell cytoplasm (day 7). Additionally, the administration of betaine prevented the reduction of Golgi complexes and mitochondrial figures in the cytoplasm observed after the exposures to CCl4. Also, the volume density of mitochondria was smallest in the CCl4-group, but the difference was not statistically significant. The results indicate that oral betaine either improves recovery or reduces the toxic effects of CCl4 on cell organelles in liver cells of male Han-Wistar rats.