麦角甾甙对实验动物消化功能的影响

麦角甾甙（10mg/kg、50mg/kg）给动物连续灌胃数天可加强正常小鼠胃排空和肠推进性蠕动,拮抗新斯的明引起的胃肠运动亢进和吗啡引起的胃肠运动抑制;麦角甾甙能提高正常大鼠胃蛋白酶活性,但对胃液分泌量和胃总酸度无明显影响;麦角甾甙可加强在体兔回盲部肠管和直肠的收缩力。     

杜香不同提取部位的镇痛抗炎作用研究

采用小鼠醋酸扭体法和角叉菜胶致小鼠足掌肿胀模型筛选杜香三种提取部位镇痛抗炎作用.结果显示,甲醇提取物(10.0、1.0 mg/kg)和水提物(10.0 mg/kg)能显著抑制醋酸引起的小鼠扭体反应和角叉菜胶引起的小鼠足趾水肿.水提物(10.0 mg/kg)在致炎后2～4 h内效果接近吲哚美辛.高效液相色谱结果提示甲醇提取物的镇痛抗炎效果可能通过其所含黄酮类化合物实现.     

小檗碱的消炎镇痛作用

皮下注射小檗碱明显减少醋酸性小鼠扭体反应次数,半数有效量为3.5mg/kg,仅在皮下注射8mg/kg的大剂量时,对热板法实验表现出镇痛作用。口服60mg/kg 小檗碱明显抑制醋酸提高小鼠腹腔毛细血管通透性;皮下注射20和50mg/kg都显著抑制组胺提高大鼠皮肤毛细血管通透性。给小鼠皮下注射4和8mg/kg小檗碱显著抑制二甲苯引起耳壳肿胀;给大鼠皮下注射20和40mg/kg时显著抑制角叉菜胶引起的足跖肿胀,作用持续7小时以上。小檗碱的消炎镇痛作用随剂量增大而增加。     

吗啡耐受对小鼠胃肠推进运动的影响

以炭末胶液在小鼠小肠推进距离占小肠全长的百分数为指标,研究了吗啡耐受对胃肠推进运动的影响。结果如下:(1)吗啡有抑制正常小鼠胃肠推进运动的作用,且随着吗啡剂量的增加,抑制作用逐渐加强。当吗啡剂量为1.25mg/kg 时,推进距离为全小肠的45%,当吗啡剂量增至4倍和16倍时,推进距离分別减少至全小肠的13.5%和6.4% 。(2)吗啡对胃肠推进运动的抑制作用,可因注射纳洛酮而阻断。(3)反复注射吗啡12天,测痛试验表明已产生耐受的动物,吗啡对胃肠推进运动的抑制效应减弱或消失,表明胃肠推进运动也能对吗啡产生耐受。(4)小鼠胃肠对吗啡产生耐受是逐步发展的。从重复注射吗啡4天时起,吗啡对胃肠推进的抑制作用即行减弱,其推进距离为对照组的2.2倍,表明已产生耐受。同法注射吗啡16天,吗啡对胃肠推进运动的抑制作用即消失,推进距离为对照组的11.8倍。但当停止注射吗啡后,胃肠耐受逐渐消退,表明耐受过程是可逆的。     

低剂量三聚氰胺对小鼠精子质量影响的研究

采用灌胃法,研究了三聚氰胺在1.0 mg/kg、2.0 mg/kg、4.0 mg/kg浓度下染毒35 d时,小鼠体重、精子运动参数和精子形态的变化.结果显示,4.0 mg/kg 处理组小鼠部分精子运动参数显著性降低(P＜0.05),1.0 mg/kg 和2.0 mg/kg 浓度组各项精子运动参数与对照比较变化不显著(P＞0.05);在染毒一周后,2.0 mg/kg 浓度组小鼠体重增长显著性下降(P＜0.05),4.0 mg/kg 浓度组小鼠体重极显著降低(P＜0.01);3个处理浓度组对小鼠精子形态影响均不显著.总之,食物中低浓度三聚氰胺对小鼠精子活性和形态无明显的影响.     

贯叶连翘提取物对小鼠抗应激反应及运动力竭小鼠抗氧化活性的影响

目的：研究贯叶连翘提取物（HPLE）对小鼠抗应激反应及运动力竭小鼠抗氧化活性的影响。方法：ICR小鼠,雌雄各半,随机均分为生理盐水（NS）对照组及高、中、低剂量HPLE组。分别采用负重游泳、常压耐缺氧和耐低温实验,观察小鼠抗急性应激反应能力,HPLE组分别按1.5 g/kg、0.75 g/kg和0.38 g/kg,ig,Bid,连续给药7 d;NS组等体积生理盐水ig。另取ICR小鼠40只,雌雄各半。随机均分为NS对照组及HPLE高、中、低剂量组。分别按ig HPLE 1.5 g/kg、0.75 g/kg和0.38 g/kg,q.d;对照组：ig等量NS,qd。连续用药2周后,开始每天进行游泳训练0.5 h,到第21天后,游泳力竭后休息20 min,断头取血,制备血清,检测小鼠血清中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性和丙二醛（MDA）的含量变化。结果：HPLE可延长小鼠负重游泳时间,缺氧存活时间及提高耐低温能力,并能升高运动力竭小鼠血清中SOD和GSH-Px活性,降低MDA的含量。结论：HPLE可提高小鼠应激反应能力,并具有抗氧化活性。     

当归不同提取液中阿魏酸、咖啡酸含量及抗氧化作用的比较研究北大核心CSCD

为考察不同提取条件对当归提取液中阿魏酸和咖啡酸的含量及抗氧化作用的影响,本研究通过HPLC外标一点法检测当归提取液中阿魏酸和咖啡酸的含量,通过DPPH法和ABTS法检测当归提取液的抗氧化作用。研究结果表明,不同提取条件下当归提取液中阿魏酸的含量为0. 574～0. 707 mg/g,咖啡酸为0. 012～0. 082 mg/g;碱水溶液提取时阿魏酸与咖啡酸的含量最高,其抗氧化活性也最强,而95%乙醇提取时的含量最低,抗氧化活性最弱;提取溶剂随醇浓度的增加,咖啡酸的含量逐渐减少,阿魏酸的含量呈现先增加后减少的趋势,30%～50%乙醇提取时各组分有良好的协同抗氧化作用。     

当归不同提取液中阿魏酸、咖啡酸含量及抗氧化作用的比较研究

为考察不同提取条件对当归提取液中阿魏酸和咖啡酸的含量及抗氧化作用的影响,本研究通过HPLC外标一点法检测当归提取液中阿魏酸和咖啡酸的含量,通过DPPH法和ABTS法检测当归提取液的抗氧化作用。研究结果表明,不同提取条件下当归提取液中阿魏酸的含量为0. 574～0. 707 mg/g,咖啡酸为0. 012～0. 082 mg/g;碱水溶液提取时阿魏酸与咖啡酸的含量最高,其抗氧化活性也最强,而95%乙醇提取时的含量最低,抗氧化活性最弱;提取溶剂随醇浓度的增加,咖啡酸的含量逐渐减少,阿魏酸的含量呈现先增加后减少的趋势,30%～50%乙醇提取时各组分有良好的协同抗氧化作用。     

阿魏酸对刀豆蛋白A诱导的小鼠免疫性肝损伤的保护作用

探讨阿魏酸(ferulic acid, FA)对刀豆蛋白A (concanavalin A, Con A)诱导的免疫性肝损伤是否有保护作用。将雄性Balb/c小鼠随机分成6组:空白组、阿魏酸对照组(100 mg/kg)、模型组(15 mg/kg Con A)、低剂量阿魏酸干预组(10 mg/kg)、中剂量阿魏酸干预组(30 mg/kg)、高剂量阿魏酸干预组(100 mg/kg)。阿魏酸灌胃后,尾静脉注射刀豆蛋白A 15 mg/kg,24 h后,取其血和肝组织进行检测。与空白组比较,模型组中苏木精和伊红染色(HE)坏死区域明显增加,丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)水平、半胱天冬氨酸酶3 (Caspase-3)活性、肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ)水平、CD4~+T细胞中CD69的表达都明显增高。与模型组相比,阿魏酸干预组的ALT和AST水平明显降低,呈剂量依赖性,HE坏死区域减少,Caspase-3活性、TNF-α和IFN-γ水平、CD4~+T细胞CD69的表达都明显降低,且具有统计学意义。表明阿魏酸对刀豆蛋白A诱导的免疫性肝损伤有保护作用,其机制可能是抑制CD4~+T淋巴细胞的活化、细胞因子的释放,减轻炎症和肝组织的凋亡。     

嗜酸乳杆菌耗尽培养上清液对小鼠在体肠管运动的影响

目的研究嗜酸乳杆菌LA14菌株耗尽培养上清液(spent culture supernatant,SCS)对小鼠在体肠管运动的影响。方法昆明种小鼠50只,随机分为5组。各组分别灌胃给予SCS、活菌菌液、SCS+活菌菌液25ml/(kg.次)、硫酸阿托品注射液10 mg/(kg.次)和等容积生理盐水,每天2次,连续3 d。末次给药后1 h,各组灌胃给予印度墨汁0.2 ml/只,20 min后处死,测定小肠全长及墨汁在小肠内推进距离,计算墨汁推进率和抑制率。另取小鼠60只,随机分为6组。各组分别灌胃给予SCS、活菌菌液、SCS+活菌菌液25 ml/(kg.次)、思密达散剂1.5 g/(kg.次)或等容积生理盐水,每天2次,连续3 d。末次给药后1 h,除生理盐水组外,其余各组灌胃给予甲硫酸新斯的明注射液2 mg/kg,10 min后各组灌胃给予印度墨汁0.2 ml/只,10 min后处死,同上述方法进行测定与计算。结果在SCS组、SCS+活菌组及阿托品组,正常小鼠的墨汁推进率明显降低,与生理盐水组比较差异有非常显著性(P0.01)。给予新斯的明造模后,小鼠的肠蠕动亢进,墨汁推进率明显升高,与生理盐水组比较差异有非常显著性(P0.01),而给予SCS、活菌、SCS+活菌以及思密达后,由新斯的明所造成的小鼠小肠运动亢进受到明显抑制,小鼠墨汁推进率显著下降,与模型组比较差异有非常显著性(P0.01)。结论嗜酸乳杆菌SCS能显著抑制正常小鼠的小肠推进运动;同时SCS及活菌能明显拮抗新斯的明所致的小鼠小肠运动亢进。     

复方银杏胶囊镇痛作用及其机制的实验研究

目的:研究复方银杏胶囊的镇痛作用及其机制.方法:大鼠电刺激法测定痛阈;用试剂盒比色法测定脑组织中谷氨酸的含量;原子吸收光谱法测定脑组织中钙离子(Ca2 )浓度;免疫组织化学ABC法观察脑组织中N-甲基-D-天门冬氨酸Ⅰ型受体(NMDAR1)的分布.结果:复方银杏胶囊350 mg/kg可显著提高大鼠电刺激嘶叫阈(P＜0.05),700 mg/kg显著减少小鼠脑组织中谷氨酸的释放以及脑内钙离子浓度(P＜0.05);复方银杏胶囊700 mg/kg、350 mg/kg可明显减少疼痛模型小鼠大脑皮层NMDAR1阳性细胞数(P＜0.01,P＜0.05).结论:复方银杏胶囊具有良好的镇痛效应,其镇痛作用可能与拮抗NMDA受体从而抑制脑组织中谷氨酸的释放及钙离子内流有关.     

Radiation protection of DNA by ferulic acid under in vitro and in vivo conditions

The effect of ferulic acid was studied on γ-radiation-induced relaxation of plasmid pBR322 DNA and induction of DNA strand breaks in peripheral blood leukocytes and bone marrow cells of mice exposed to whole body γ-radiation. Presence of 0.5 mM ferulic acid significantly inhibited the disappearance of supercoiled (ccc) plasmid pBR322 with a dose modifying factor (DMF) of 2.0. Intraperitoneal administration of different amounts (50, 75 and 100 mg/kg body weight) of ferulic acid 1 h prior to 4 Gy γ-radiation exposure showed dose-dependent decrease in the yield of DNA strands breaks in murine peripheral blood leukocytes and bone marrow cells as evidenced from comet assay. The dose-dependent protection was more pronounced in bone marrow cells than in the blood leukocytes. It was observed that there was a time-dependent disappearance of radiation induced strand breaks in blood leukocytes (as evidenced from comet parameters) following whole body radiation exposure commensuration with DNA repair. Administration of 50 mg/kg body weight of ferulic acid after whole body irradiation of mice resulted disappearance of DNA strand breaks at a faster rate compared to irradiated controls, suggesting enhanced DNA repair in ferulic acid treated animals. (Mol Cell Biochem xxx: 209–217, 2005)     

Synergistic interactions of Ferulic acid with Ascorbic acid: Its cardioprotective role during isoproterenol induced myocardial infarction in rats

Studies on the lipid peroxidation and antioxidant changes and their significance during myocardial injury have provided a new insight into the pathogenesis of heart disease. The heart failure subsequent to myocardial infarction may be associated with an antioxidant deficit as well as increased myocardial oxidative stress. The present study was designed to evaluate the effect of the combination of ferulic acid and ascorbic acid on antioxidant defense system and lipid peroxidation against isoproterenol (ISO)-induced myocardial infarction in rats. Induction of rats with isoproterenol (150 mg/kg body weight daily, i.p.) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT), and a significant decrease in activities of endogenous antioxidants (SOD, GPx, GST, CAT, and GSH). Pre-co-treatment with the combination of ferulic acid (20 mg/kg body weight/day) and ascorbic acid (80 mg/kg body weight/day) orally for 6 days, significantly attenuated these changes when compared to the individual treatment groups. Histopathological observations were also in correlation with the biochemical parameters. Thus, ferulic acid and ascorbic acid significantly counteracted the pronounced oxidative stress effect of ISO by the inhibition of lipid peroxidation, restoration of antioxidant status, and myocardial marker enzymes levels. In conclusion, these findings indicate the synergistic protective effect of ferulic acid and ascorbic acid on lipid peroxidation and antioxidant defense system during ISO-induced myocardial infarction and associated oxidative stress in rats.     

EFFECTS OF CHRONIC TREATMENT WITH AMINO-OXYACETIC ACID OR SODIUM n-DIPROPYLACETATE ON BRAIN GABA LEVELS AND THE DEVELOPMENT AND REGRESSION OF COBALT EPILEPTIC FOCI IN RATS

Abstract– Acute treatment of cobalt-induced epilepsy in rats with amino-oxyacetic acid (20-60 mg/kg intraperitoneally) resulted in a short period (30-90 min) of epileptic spike suppression. In contrast sodium n -dipropylacetate (100-400 mg/kg intraperitoneally) had no effect on spike frequencies. Chronic treatment of cobalt epileptic rats with amino-oxyacetic acid (2.5-10 mg/kg intraperitoneally daily) or sodium n -dipropylacetate (200-400 mg/kg intraperitoneally daily) elevated brain GABA concentrations significantly and reduced brain glutamate decarboxylase activity relative to control saline-injected cobalt epileptic rats. Brain γ-aminobutyrate aminotransferase activity was significantly reduced by chronic treatment with amino-oxyacetic acid, whereas chronic sodium n -dipropylacetate had no effect on brain γ-aminobutyrate aminotransferase activity although elevating brain GABA. Amino-oxyacetic acid (2.5-10 mg/kg intraperitoneally per day) reduced the frequency of epileptic spikes in the secondary foci of cobalt epileptic rats. The anticonvulsant action of amino-oxyacetic acid was most marked at 5 mg/kg intraperitoneally where a secondary focus failed to develop in treated cobalt epileptic rats. However, there was no simple relationship between the elevation of brain GABA and the anticonvulsant action of amino-oxyacetic acid. Thus focal GABA was higher in rats given intraperitoneal amino-oxyacetic acid (10 mg/kg) but the anticonvulsant action of amino-oxyacetic acid was less marked at this dose. Sodium n -dipropylacetate (200-400 mg/kg intraperitoneally per day) had no long-term anticonvulsant action in this model of epilepsy. It is concluded that the anticonvulsant action of sodium n -dipropylacetate, and probably that of amino-oxyacetic acid, is not likely to be mediated through a mechanism involving elevation of brain GABA.     

灵芝对小鼠空间分辨学习与记忆的影响

本文用Y-型迷宫法测试小鼠空间分辨行为。实验结果表明,每日ig灵芝2.58/kg共7d,有明显促进学习的作用。每日ig灵芝2.5g/kg共7d或ig灵芝5g/kg共7d都能显著地拮坑东莨菪碱所致学习障碍的作用。此外,学习训练后立即ig灵芝2.5g/kg或ig灵芝5g/kg也有明显地改善东莨菪碱损害记忆巩固的作用。     

阿魏酸对糖尿病小鼠心肌病变的影响及其机制

目的：研究阿魏酸对高脂饮食结合小剂量链脲佐菌素（STZ）诱导的2型糖尿病小鼠心肌病变的影响,探讨其可能的作用机制。方法：雄性ICR小鼠20只,高糖高脂饮食连续6周,STZ （30 mg/kg）腹腔注射连续5d后,隔9d测空腹血糖（FBG）,超过11.1 mmol/L视为糖尿病造模成功。将此20只小鼠随机分为模型组、阿魏酸组（200 mg/kg,i.g.）,每组10只;另取10只正常小鼠为对照组;连续给药8周。末次给药后,测定FBG、称体重、全心重和左心室重,计算心脏质量指数（HMI）和左室质量指数（LVMI）;测定超氧化物歧化酶（SOD）活力、丙二醛（MDA）含量;Masson染色观察左心室纤维增生情况;免疫组化法测定心肌组织转化生长因子-β1（TGF-β1）、Ⅲ型胶原蛋白表达。结果：与模型组小鼠比较,阿魏酸组小鼠HMI、LVMI减小（（P<0.01,P<0.05）,心肌组织SOD活力升高、MDA含量下降（P<0.05）;心肌胶原纤维沉积减少,间质纤维化改善;免疫组化显示心肌组织TGF-β1和Ⅲ型胶原蛋白表达减少（P<0.01,P<0.05）。结论：阿魏酸对糖尿病小鼠心肌病变具有保护作用,可能与抗氧化及抑制TGF-β1蛋白表达,减少Ⅲ型胶原蛋白沉积有关。     

野生地参多糖对四氧嘧啶致糖尿病小鼠血糖和血脂的影响

为了研究野生地参多糖对四氧嘧啶(ALX)致糖尿病小鼠血糖和血脂的影响,利用四氧嘧啶(ALX)建立糖尿病小鼠模型,分别灌胃低(100 mg/(kg.d))、中(200 mg/(kg.d))、高(400 mg/(kg.d))剂量地参多糖溶液及阳性对照药盐酸苯乙双胍,正常对照组及糖尿病模型对照组则给等体积生理盐水。结果表明:连续给药14 d后,地参多糖对正常小鼠血糖无明显影响,100、200和400 mg/(kg.d)地参多糖均能明显降低ALX所致糖尿病小鼠高血糖,与糖尿病模型对照组相比,P<0.01;同时,相同剂量的地参多糖还能极显著降低ALX致糖尿病小鼠血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)(P<0.01)。中、高剂量地参多糖使糖尿病小鼠血清高密度脂蛋白胆固醇(HDL-C)显著回升(P<0.05),但低剂量地参多糖对糖尿病小鼠血清HDL-C则无明显影响(P>0.05)。地参多糖能明显降低ALX致糖尿病小鼠高血糖及高血脂。     

Effect of resiniferatoxin on stimulated gastric acid secretory responses in the rat

The effect of the capsaicin analogue ‘resiniferatoxin’ (RTX) was studied on basal and stimulated gastric acid secretory responses following sc bethanechol (1.5 mg/kg), sc pentagastrin (50 μg/kg) and sc histamine (0.5 and 2.5 mg/kg) in the 1-h pylorusligated plus saline (2 ml ig)-treated rats. Resiniferatoxin applied intragastrically in doses of 0.6 and 1 μg/kg at time of pylorus-ligation and administration of the above secretagogues reduced acid secretory respones to bethanechol by 18.3 and 26.4%, to 0.5 mg/kg histamine by 39.9 and 44.6%, to 2.5 mg/kg histamine by 21.3 and 40.8% and to pentagastrin by 10.2 and 30.9% respectively. A single sc injection of 0.4 μg/kg of RTX abolished basal secretion in pylorus ligated rats (which did not receive ig saline). Our results indicate that locally applied RTX is capable of inhibiting basal secretory responses and modifying gastric acid responses stimulated with histamine, bethanechol or pentagastrin in the rat.     

N-Terminal Amino Acid Sequence of the Chlorophyll-binding Protein CP-47 of Photosystem 2 in the Thermophilic Cyanobacterium Synechococcus elongatus

Effects of caffeic acid and chlorogenic acid on mutagenicity were studied using the Salmonella typhimurium system. These compounds had inhibitory effects on the mutagenicity of Trp-P-1 and Glu-P-2. Caffeic acid completely eliminated the mutagenicity induced by activated Glu-P-2. Some compounds analogous to caffeic acid, such as cinnamic acid, coumaric acid, and ferulic acid, also significantly decreased the mutagenicity of Glu-P-2.