Antiarrhythmic effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia/reperfusion injury in rats

OBJECTIVES: The present study was designed to determine the antiarrhythmic effect of caffeic acid phenethyl ester (CAPE), an active component of propolis, which exhibits antioxidant properties, in rats subjected to myocardial ischemia and ischemia-reperfusion (I/R) injury. DESIGN AND METHODS: Rats were subjected to 30 min coronary artery occlusion for evaluating the effect of CAPE on the myocardial ischemia injury. While in the myocardial I/R injury study, the coronary artery was ligated for a 5-min period of ischemia followed by a 30-min period of reperfusion. Animals were pretreated with or without CAPE before coronary artery ligation and the severity of myocardial ischemia- and I/R-induced arrhythmias and mortality were compared. RESULTS: Pretreatment of CAPE (0.1 and 1 microg/kg) not only reduced both the incidence and duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) but also decreased the mortality during the myocardial ischemia and I/R injury period. CONCLUSIONS: Our results suggest that CAPE is a potent antiarrhythmic agent with cardioprotective effects in myocardial ischemia and I/R injury rats.     

Effects of melatonin and caffeic acid phenethyl ester on testicular injury induced by myocardial ischemia/reperfusion in rats

Experimental studies indicate that ischemia/reperfusion (I/R) causes remote organ injury although the molecular mechanism has not been clearly defined. In this report, the role of oxidative injury on testicular damage following myocardial I/R injury and the effects of antioxidant agents, melatonin and caffeic acid phenethyl ester (CAPE), on testicular injury were investigated. As far as we know, this is the first report demonstrating that myocardial I/R induces damage to the testes. Thirty-two male Wistar rats were randomly divided into four groups: sham operation (SO), I/R + vehicle, I/R + melatonin, and I/R + caffeic acid phenethyl ester. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Serum nitric oxide (NO) and malondialdehyde (MDA) levels and morphological changes were examined. I/R was accompanied by a significant increase in serum MDA and NO levels, whereas, melatonin and CAPE administration significantly reduced these values. Melatonin was more efficient in reducing MDA levels than CAPE (P < 0.05). I/R induced myocardial damage, manifested as the histopathological evidence of intracellular vacuolization, interstitial edema, neutrophil infiltration and coagulative necrosis. I/R + vehicle group showed many histological alterations such as focal tubular atrophy, and degeneration and disorganization of the seminiferous epithelium in testes. The number of atrophic tubules and degenerating cells was significantly higher in I/R + vehicle group than that of SO group. Melatonin and CAPE significantly reduced the number of degenerating cells; additionally, melatonin reduced the number of atrophic tubules (P < 0.05). Our results indicate that myocardial I/R induces severe testicular damage and antioxidant agents, especially melatonin, have protective effects on testicular injury after myocardial I/R. Our data emphasize that oxygen-based reactants may play a central role in remote organ injury.     

咖啡酸苯乙酯对白化病大鼠视网膜光损伤的保护研究

目的从形态和功能两方面测试咖啡酸苯乙酯（CAPE）是否能够保护视网膜组织免于光损伤诱导的氧化损伤。方法分别将大鼠暴露于50 lx循环暗光2周、50 lx循环暗光8周、200 lx循环明光8周,同时给予0.01%CAPE和对照饲料喂养;以ERG和组织学分别检测大鼠视网膜对循环暗光和循环明光的反应。结果不论是喂养2周还是喂养8周,在循环暗光下,CAPE组ERG A/B波幅均显著高于对照组（P〈0.05）;在循环明光下,ERGA/B波幅CAPE组和对照组之间差异无统计学意义（P〉0.05）;上述三组组织学结果差异均无统计学意义。结论 PE可以在循环暗光下保护视网膜功能。CAPE有可能作为一种天然化合物保护白化病或者其他视网膜变性患者视网膜功能。     

Protective role of caffeic acid phenethyl ester in the liver of rats exposed to cold stress

Cold exposure can induce a form of environmental stress. Cold stress (CS) alters homeostasis, results in the creation of reactive oxygen species and leads to alterations in the antioxidant defense system. The caffeic acid phenethyl ester (CAPE), an active component of propolis, has an antioxidant capacity. We investigated the effect of CS on oxidative stress and antioxidant defense system and the possible protective effect of CAPE in rat liver tissue. Twenty-four female Wistar Albino rats were divided into four groups: Control, CAPE-treated, CS, and CAPE-treated CS (CS + CAPE) group. Catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) activities and total glutathione (GSH) and malondialdehyde (MDA) levels were measured. In addition, histological changes in liver tissue were examined by light microscopy. SOD, CAT and GSH-Px activities and total GSH level were significantly declined in the CS group. In the CS + CAPE group, the activities of these three enzymes and GSH level significantly raised with regard to the CS group. MDA levels increased in the CS group and decreased in the CS + CAPE group. The tissues of the CS group showed some histopathological changes such as necrosis, hepatocyte degeneration, sinusoidal dilatation, hemorrhage and vascular congestion and dilatation. In the CS + CAPE group, the histopathological evidence of hepatic damage was markedly reduced. Histological parameters were consistent with biochemical parameters. In this study, CS increased oxidative stress in liver tissue. CAPE regulated antioxidant enzymes, inhibited lipid peroxidation and reduced hepatic damage.     

The effects of caffeic acid phenethyl ester and melatonin on age-related vascular remodeling and cardiac damage

Oxidative stress has been implicated with cardiovascular aging. Most antioxidant intervention studies have involved long-term treatments as a potential means to eliminate age-related oxidative damage in many systems. In the present study, not only light and electron microscopic pictures of the heart and thoracic aorta of young and aged and, caffeic acid phenethyl ester (CAPE) and melatonin and administered aged Sprague Dawley rats, but also antioxidant system status was evaluated. Significantly elevated levels of malondialdehyde (MDA) were observed in the heart and thoracic aorta of aged rats (P<0.05 and P<0.001, respectively). Chronic melatonin and CAPE administration significantly reduced the levels of MDA in the heart (P=0.005 and P=0.05, respectively) and thoracic aorta (P<0.001 and P<0.05, respectively) of aged animals. Additionally, melatonin and CAPE were efficient in stimulating the activities and increasing the levels of the antioxidant enzymes in the heart and aorta. Prominent electron microscopic alterations in cardiac myocytes such as nuclear irregularity, mitochondrial degeneration, myofilament disorganization and disruption, and lipofuscin accumulation were observed in aged rats. The main age-related histologic modifications observed in aorta were irregularity in endothelial cells and their nuclei, divergence of endothelial cells from basement membrane and neighboring cells, and elastic fibril fragmentation and reduction. Melatonin and CAPE obviously reduced these alterations in both heart and aorta of aged rats. Taking the results together, we suggest that supplemental administration of CAPE and melatonin is beneficial in delaying age-related cellular damage in cardiovascular system.     

Caffeic acid phenethyl ester protects against oxidative stress-related renal dysfunction in rats treated with cyclosporin A

The therapeutic index of cyclosporin A (CsA), an immunosuppressive drug, is limited by its nephrotoxic effect. Oxidative stress is suggested to play a crucial role as pathogenic factors. The present study aimed at investigating the effects of caffeic acid phenethyl ester (CAPE), a phenolic antioxidant, on renal function, morphology, and oxidative stress following CsA treatment. Rats were treated with vehicle, CsA (50 mg/kg), and CsA plus CAPE (10 and 30 μmol/kg) for 10 days. Renal function, histopathology, and tissue malondialdehyde (MDA) and reduced glutathione (GSH) levels were evaluated 24 h after the last treatment. CsA produced nephrotoxicity as indicated by a significant increase in serum creatinine and blood urea nitrogen, but decrease creatinine and urea clearance compared to those treated with vehicle. Severe vacuolations and tubular necrosis were evident in the kidney of CsA-treated rats. CsA also increased renal MDA and decreased GSH content significantly. Administration of CAPE along with CsA restored all the changes caused by CsA. These results clearly demonstrate the pivotal role of oxidative stress and its relation to renal dysfunction and also point to the protective potential of CAPE against CsA nephrotoxicity. The protection afforded by CAPE is mediated, at least in part, through inhibiting renal lipid peroxidation and enhancing or maintaining the antioxidant glutathione content.     

Myocardial ischemia/reperfusion-induced oxidative renal damage in rats: protection by caffeic acid phenethyl ester (CAPE)

Myocardial ischemia-reperfusion (MI/R) may induce renal damage. A rat model of M/IR injury was established. The left coronary artery was clamped for 30 min, constituting the ischemic period, and was then released for 120 min, thus constituting the reperfusion period. The purpose of this study was to evaluate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant, on renal dysfunction in rats undergoing MI/R. CAPE (50 mumol/kg) was administered by infusion 10 min before ischemia and during occlusion. Hemodynamic changes were recorded during the different periods. At the end of the reperfusion period, rats were sacrificed, and the kidneys were quickly removed for biochemical determination and histopathological analysis. MI/R was accompanied by a significant increase in malondialdehyde (MDA) production and decrease in glutathione (GSH) content in the rat kidney. Administration of CAPE reduced MDA production and prevented depletion of GSH content. These beneficial changes in these biochemical parameters were also associated with parallel changes in histopathological appearance. These findings imply that MI/R plays a causal role in kidney injury through overproduction of oxygen radicals or insufficient antioxidant, and CAPE exerts renal-protective effects probably by its radical scavenging and antioxidant activities.     

Effects of caffeic acid phenethyl ester on lipid peroxidation and antioxidant enzymes in diabetic rat heart

OBJECTIVES: The risk for cardiovascular disease is significantly high in diabetes mellitus. Experimental evidence suggests that oxidative stress plays a dominant role in the pathogenesis of diabetes mellitus. Caffeic acid phenethyl ester (CAPE), an active component of propolis, has several biological and pharmacological properties, including antioxidant, anti-inflammatory, anti-carcinogenic, antiviral, and immunomodulatory activities. In light of the antioxidant ability of CAPE, the effects of CAPE on the antioxidative status of cardiac tissue were investigated in streptozotocin (STZ)-induced diabetic rats. DESIGN AND METHODS: Twenty-six rats were randomly divided into three groups: group I, control, nondiabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 7); and group III, STZ-induced, CAPE-treated diabetic rats (n = 10). In groups II and III, diabetes developed 3 days after intraperitoneal (ip) administration of a single 35 mg kg(-1) dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10 mumol kg(-1) ip dose of CAPE per day. After 8 weeks, the levels of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the cardiac tissues of all groups were analyzed. RESULTS: In untreated diabetic rats, MDA markedly increased in the cardiac tissue compared with the control rats (P < 0.05). However, MDA levels were reduced to the control level by CAPE. The activities of SOD and CAT in the untreated diabetic group and the CAPE-treated diabetic group were higher than those of the control group (P < 0.05). Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats in the untreated diabetic group (P < 0.05). There were no significant differences in the activity of GSH-Px between the rats in the untreated diabetic group and the control group. However, the activity of GSH-Px was increased in CAPE-treated diabetic rats compared with the control and untreated diabetic rats (P < 0.05). CONCLUSION: These results reveal that diabetes mellitus increases oxidative stress in cardiac tissue and CAPE has an ameliorating effect on the oxidative stress via its antioxidant property.     

Effect of intraaortic balloon counterpulsation (IABP) on myocardial infarct size and collateral flow in an experimental dog model

To determine the influence of IABP on infarct size and collateral blood flow in each of 12 openchest anaesthetised mongrel dogs two small branches of the left coronary artery were occluded consecutively. The perfusion areas of both branches were comparable in size. IABP was started immediately before ligation of the first branch for a 90-min period followed by a reperfusion period of 90 min. Subsequently the second vessel was also occluded for 90 min as a control without IABP while myocardial oxygen consumption remained constant and was then reperfused. Infarct size was expressed as a percentage of the perfusion area. A difference in infarct size with and without IABP (18±17, 18±10% respectively) could not be observed. However a significant increase of collateral blood flow due to IABP in the subendocardial layer from 8.9±4.8 to 14.9±4.6 ml/100 g/min (p<0.05) was prevalent. In the subepicardial layer the augmentation from 23.7±19.9 to 26.9±15.2 was not significant. Thus, in spite of a small increase of collateral blood flow in the subendocardial layer of the ischemic myocardium the infarct size was not reduced by IABP in our dog model.     

不同剂量重组人促红细胞生成素对心肌梗死大鼠血流动力学和梗死面积的影响

目的 探讨不同剂量重组人促红细胞生成素(recombinant human erythropoietin,rHu-EPO)对心肌梗死大鼠血流动力学和左室梗死面积的影响.方法 选取成年SD大鼠64只,随机分为假手术组、心肌梗死对照组、大剂量治疗组和小剂量治疗组.各组分别于术后24 h和2周检测血流动力学指标和左室梗死面积.结果 术后24 h:与假手术组相比,心肌梗死对照组LVSP、LVEDP和±dp/dt_(max)显著恶化;与心肌梗死对照组相比,大、小剂量治疗组±dp/dt_(max)有显著改善.术后2周:与假手术组相比,心肌梗死对照组LVSP、LVEDP和±dp/dt_(max)显著恶化;与心肌梗死对照组相比,大、小剂量治疗组±dp/dt_(max)有显著改善,梗死面积显著缩小;与大剂量治疗组相比,小剂量治疗组±dp/dt_(max)有显著改善.结论 心肌梗死后即刻给予大剂量rHu-EPO,并术后减量维持治疗1周可明显缩小梗死面积,保护心功能,小剂量维持治疗的改善心功能效果更好.     

蓝光对维甲酸致骨质疏松大鼠的影响

目的：探讨蓝光照射后维甲酸致大鼠骨质疏松模型的骨代谢指标及骨微结构的改变情况。方法：将24只9月龄SD大鼠随机分为正常组、模型组、蓝光1组和蓝光2组，每组6只。蓝光组和模型组每天用100 mg/kg的维甲酸连续灌胃14 d，正常组用同体积的蒸馏水灌胃14 d，14 d后各组均恢复正常饮食、饮水。正常组和模型组全程采用日光灯光照模式照射，蓝光1组和2组在维甲酸造模完成后分别采用蓝色光照模式（460 nm）照射14 d和21 d。非蓝光照射时日光灯照射补齐至总照射天数（35 d）。所有大鼠均于35 d后取眼眶血，测定血清钙、磷、碱性磷酸酶（alkaline phosphatase，ALP）、β-胶联降解物（β-bonded degradation products，β-CTX）和Ⅰ型前胶原氨基端肽（amino terminal peptide of procollagen type 1，P1NP）水平。采用CO₂麻醉处死大鼠后取股骨，用microCT测定骨密度、骨小梁数量、骨小梁厚度和骨小梁分离度。结果：与正常组相比，模型组钙、磷、ALP、β-CTX和P1NP水平以及骨密度、骨微结构显著改变（P<0.01），说明造模成功。与模型组相比，蓝光1组的体质量、血钙水平、血磷水平、ALP、β-CTX，P1NP、骨小梁数量、骨小梁厚度、骨小梁分离度发生显著变化（P<0.05），但两组骨密度差异无统计学意义；蓝光2组大鼠的体质量、骨密度、骨微结构及骨代谢等各项指标均改变（P<0.05）。蓝光1组和蓝光2组间β-CTX、骨小梁数量和骨小梁分离度差异均有统计学意义（P<0.05）。结论：蓝光可在大鼠骨质疏松早期抑制成骨和影响钙磷代谢，促进维甲酸诱导骨质疏松的进程，提示骨质疏松患者在日常生活中需要减少蓝光暴露。     

吡咯喹啉醌对NMDA诱发大鼠海马神经元损伤的影响

目的探讨吡咯喹啉醌（PQQ）对N-甲基-D-天冬氨酸（NMDA）诱发海马神经元损伤的影响。方法体外原代培养新生大鼠海马神经元，毒性剂量的NMDA诱致海马神经元损伤，预加PQQ，镜下观察神经元的形态变化，琼脂糖凝胶电泳观察细胞的死亡情况，激光共聚焦显微镜观察细胞内Ca^2＋浓度的变化。结果体外培养8d的海马神经用0．1mmol／LNMDA处理后，细胞内Ca^2＋快速增加，细胞以坏死和凋亡两种形式死亡，细胞的存活率降低；预先给予PQQ可明显减少细胞内Ca^2＋的增加，减少细胞死亡。结论PQQ对NMDA诱发的海马神经元损伤具有保护作用。     

硫辛酸在急性百草枯中毒致心肌损伤中保护作用的实验研究

目的：观察抗氧化剂硫辛酸对急性百草枯中毒造成的心肌损伤,心肌组织中NF-κB、NOS、NO及血中心肌酶谱的变化的影响,探讨硫辛酸对百草枯中毒所致心肌损伤的可能保护机制。方法：选择健康雄性Sprage-Dawley大鼠126只,随机分4组：正常对照组（NS）、百草枯中毒组（PQ）、百草枯＋还原型谷胱甘肽组（GSH）、百草枯＋硫辛酸治疗组（LA）。NS组6只;PQ组和GSH组各24只;LA组72只,再细分3个亚组,即30mg/kg、60mg/kg、100mg/kg亚组,每亚组24只。NS组给予生理盐水灌胃;PQ组给予PQ 50mg/kg灌胃;GSH组给予PQ 50mg/kg灌胃,半小时后给予GSH 200mg/kg/d腹腔注射,连续6d;LA组给予PQ 50mg/kg灌胃半小时后分亚组给予LA 30mg/kg/d、60mg/kg/d、100mg/kg/d腹腔注射,连续6d。于造模成功后1d、3d、5d、7d取大鼠相同部位的心肌组织HE染色,光镜下观察组织学变化;取另外相同部位心肌组织检测NF-κB、NOS、NO水平;腹主动脉取血检测AST、LDH、CK、CKMB水平。结果：①HE染色结果显示PQ组心肌破坏严重,心肌组织严重水肿,出血,点状坏死灶,组织间隙增宽,心肌细胞广泛肿胀、变性。GSH组在进行干预后出现上述情况较同时点的PQ组减轻。LA组在进行干预后出现上述情况较同时点的PQ组及GSH组少,心肌组织损伤轻,主要表现为局部嗜酸性变。随着LA剂量的增加,效果更加显著。②NF-κB水平、NOS的活力、NO水平：LA组与PQ组、GSH组的各相同时点对比均低,P〈0.01有统计学意义;LA组各时点与NS组对比均高,P〈0.05有统计学意义;随着LA剂量的增加,NF-κB水平、NOS的活力、NO水平进行性下降,各组间比,P〈0.05有统计学意义。③AST、LDH、CK、CKMB水平：LA组与PQ组、GSH组的各相同时点对比均低,P〈0.01有统计学意义;LA组各时点与NS组对比均高,P〈0.05有统计学意义;随着LA剂量的增加,AST、LDH、CK、CKMB水平进行性下降,各组间比,P〈0.05有统计学意义。结论：硫辛酸在急性百草枯中毒中能使心肌组织的损伤减轻,其机制可能是通过直接调控NF-κB、NOS、NO的水平,影响心肌组织中自由基和炎症介质的含量,从而减轻心肌水肿、出血和坏死,改善心肌细胞代谢,保护心肌组织。     

栓线法建立大脑中动脉局灶缺血实验模型对再灌注损伤的评价意义

目的为临床脑缺血研究提供更合理实用的基础研究模型。方法选用健康Wistar大鼠41只,雌雄不限,体质量250～280g,用栓线法制作大鼠大脑中动脉局灶脑缺血模型,并限定不同时间点再灌注。结果正常对照组,假手术组,缺血30min再灌注24h组未发现神经功能缺损,评分为0分。缺血90min-再灌注模型神经功能缺损评分为2.2±0.4,梗死灶部位累及皮层和基底核。缺血持续24h组评分为3.4±0.5,与缺血90min再灌注组比,t=3.797,P<0.01。结论栓线法大鼠大脑中动脉局灶脑缺血缺血90min再灌注模型更接近临床脑缺血的病程。     

Selective blockade of A(2A) receptor protects against neurotoxicity induced by kainic acid in young rats

The aim of this study was to investigate the effect of SCH 58261, a selective adenosine A(2A) receptor (A(2A)R) antagonist, on kainic acid (KA)-induced seizures in 21-day-old rats. Rats were pretreated with SCH 58261 (1 or 3 mg/kg) by intraperitoneal (i.p.) route 30 min before KA (10 mg/kg, i.p.) administration. The appearance of clonic seizures, the latency for the onset of the first clonic seizure episode, and the number of deaths induced by KA were evaluated. To test the hypothesis of the oxidative imbalance induced by KA exposure, reactive species (RS) levels, catalase (CAT), glutathione peroxidase (GPx), and glutathione S-transferase (GST) activities in the brains of rats were measured. Both doses of SCH 58261 prolonged the latency for the onset of the first clonic seizure episode. SCH 58261, at the highest dose, decreased the appearance of clonic seizures as well as the mortality rate induced by KA administration. SCH 58261, at the dose of 3 mg/kg, was also effective in protecting against alterations in oxidative stress parameters (RS levels, CAT, GPx, and GST activities) in the brains of young rats exposed to KA. Our data reveal that SCH 58261 was protective against the neurotoxicity induced by KA. Therefore, the blockade of A(2A)R might represent a novel approach for the treatment of seizures.     

γ-羟基丁酸对脑出血的保护作用的研究

目的 评价γ-羟基丁酸治疗脑出血的临床疗效及其对脑出血后脑水肿的影响。方法 60例脑出血病例随机分为γ-羟基丁酸组及对照组，两组均接受神经内科脑出血常规治疗。γ-羟基丁酸组采用γ-羟基丁酸静脉滴注，每日1次，共2周，应用欧洲卒中评分评价临床神经功能情况，利用CT测卒中灶体积。结果 γ-羟基丁酸组临床疗效明显优于对照组．治疗后与对照组相比出血灶周围脑水肿体积明显减小。结论 γ-羟基丁酸治疗脑出血有效，而且安全。     

Influence of experimental parameters on the characteristics of poly(lactic acid) nanoparticles prepared by a double emulsion method

Nanoparticles were prepared by the double emulsion method (w/o/w), using methylene chloride as an organic solvent and polyvinyl alcohol (PVA) or human serum albumin (HSA) as a surfactant. Experimental parameters such as the preparation temperature, the solvent evaporation method, the internal aqueous phase volume, the surfactant concentration and the polymer molecular weight were investigated for particle size, the zeta potential, the residual surfactant percentage and the polydispersity index. Preparation parameters leading to particles with well-defined characteristics such as an average size around 200 nm and a polydispersity index lower than 0.1 were identified. The conditions were optimized to ensure protein encapsulation: a cool temperature, a short processing time, a sufficient internal aqueous phase and careful washing. It appeared that the higher the surfactant concentration in the external aqueous phase was, the smaller the particles, the lower the polydispersity index and the higher the residual amount of surfactant were. For PVA or HSA, the agreement between the convenient surfactant concentration and its critical aggregation concentration could be emphasized. Otherwise, an increased polymer molecular weight led both to a slightly decreased particle size and to a lower polydispersity index. Moreover, multilayer adsorption of PVA which does not depend on Poly(lactic-acid) molecular weight was exhibited. Finally, the zeta potential resulted from the polymer molecular weight and the residual PVA.     

环维黄杨星D对高血压大鼠脑缺血损伤的保护作用

目的:观察中药单体环维黄杨星D(CVB-D)对易卒中型肾血管性高血压大鼠(RHRSP)脑缺血损伤的保护作用.方法:采用环形银夹造成SD大鼠的双侧肾动脉狭窄,制成RHRSP;再用线栓法制成一侧大脑中动脉闭塞(MCAO)脑缺血-再灌注模型.观察CVB-D治疗对脑缺血6 h后再灌注6、72和168 h不同时间点大鼠的神经行为、脑梗死面积及脑含水量等影响,并与生理盐水组进行对照.结果:脑缺血-再灌注6、72和168 h后,CVB-D治疗组大鼠脑含水量分别为(79.08±1.04)%、(80.84±1.27)%和(78.37±1.16)%,比同期对照组脑含水量(82.32±1.61)%、(83.88士1.48)%、(81.61士1.31)%明显下降(P＜0.05或P＜0.01);缺血-再灌注72及168 h后治疗组大鼠脑梗死面积分别为(14.41±1.26)%和(18.41±1.62)%,明显低于同期对照组脑梗死面积(21.42±1.61)%、(22.77±1.48)%(P均＜0.05).结论:CVB-D对实验性脑缺血-再灌注大鼠脑损伤有一定保护作用.     

The effect of the synthetic prostaglandin analog 15 (R) 15 methyl-PGE2 methyl ester on gastric mucosal hemorrhage induced in rats by taurocholic acid and hydrochloric acid.

The incidence of mucosal hemorrhage induced in rats by the oral administration of taurocholic acid (TCA) and hydrochloric acid (HCl) both singly and in combination was investigated. The effect of prostaglandin 15 (R) 15 methyl-PGE2 methyl ester (Me-PGE2) on the occurrence of hemorrhage induced by TCA with HCl was also studied. The incidence of hemorrhage induced by TCA (10 mM) alone and HCl (160 mM) alone was minimal and not different from that induced by the control solution. The combination of TCA (10 mM) and HCl (160 mM) produced bleeding in 67.7% of animals. The addition of 15 (R) 15 methyl-PGE2 methyl ester (9.9 micronM, corresponding to 50 microng/Kg) significantly reduced the incidence of hemorrhage induced by the combination of TCA with HCl from 67.7% to 31.3%. This suggests that this synthetic prostaglandin may be of value in conditions thought to be associated with reflux of bile into the stomach.     

中风星蒌通腑胶囊对急性脑缺血大鼠脑组织中兴奋性氨基酸的影响

目的 :探讨中风星蒌通腑胶囊治疗急性脑缺血的作用机制及与兴奋性氨基酸 ( EAA)的关系。方法 :以急性全脑缺血大鼠为模型 ,用华佗再造丸作为阳性对照 ,将 72只普通级 Wistar大鼠随机分为假手术组、模型组、华佗再造丸组及中风星蒌通腑胶囊高、中、低剂量组 ,分别灌胃并取材后 ,测定脑组织中谷氨酸 ( Glu)、天门冬氨酸 ( Asp)含量。结果 :急性脑缺血损伤后 ,模型组大鼠脑组织中 Glu、Asp含量明显升高。在降低脑组织Glu、Asp方面 ,中风星蒌通腑胶囊高、中、低剂量组均效果显著 ,与模型组比较 ,有显著差异 ( P <0 .0 5或P<0 .0 1) ;华佗再造丸组对 Glu、Asp含量影响不明显 ( P均 >0 .0 5 )。结论 :中风星蒌通腑胶囊具有降低急性脑缺血大鼠脑组织中 EAA的作用 ,而且在这方面的作用优于华佗再造丸。