脉络宁氯化钠注射液的抗脑缺血作用

目的：观察脉络宁氯化钠注射液的抗脑缺血作用，为该药治疗脑血栓形成及其后遗症等提供药理学依据。方法：大鼠大脑中动脉阻断采用电凝法；大鼠大脑中动脉缺血再灌注采用插线法；小鼠急性不完全性脑缺血采用结扎法；对脑循环的影响采用麻醉犬在体实验法.结果：该药对大鼠大脑中动脉阻断、大鼠大脑中动脉缺血再灌注以及小鼠急性不完全性脑缺血有一定改善作用；该药能降低大鼠缺血脑组织中丙二醛含量，提高超氧化物歧化酶活性；此外，该药能降低麻醉犬脑血管阻力，增加脑血流量。结论：该药有抗脑缺血作用，这一作用与其抗自由基介导的脂质过氧化和扩张脑血管有关。     

脑络通对实验性大鼠脑缺血的保护作用

脑络通胶囊能够降低不完全性脑缺血模型大鼠的脑含水量、毛细血管通透性,并且能够降低缺血脑组织过氧化脂质含量,提高过氧化物歧化酶活性。     

脑脉康对大鼠脑缺血模型神经细胞的保护作用

本研究观察了中药复方脑脉康对大鼠脑缺血模型神经细胞的影响,发现结扎动物两侧颈总动脉造成不完全性脑缺血后,脑神经细胞发生明显的变性坏死,脑组织中过氧化脂质的分解产物丙二醛含量明显增多。脑脉康能显著降低脑缺血组织中的丙二醛含量,抑制自由基反应,减少病变细胞所占的百分率,表明该药对脑缺血组织具有保护作用。     

开心散对实验性大鼠脑缺血的保护作用

开心散能够降低不完全性脑缺血模型大鼠的脑含水量、毛细血管通透性,并且能够降低缺血脑组织过氧化脂质含量,提高过氧化物歧化酶活性。     

脑康灵胶囊抗大鼠脑缺血的研究

目的观察脑康灵胶囊对脑缺血/再灌注损伤的保护作用,并对其机制作初步探讨。方法采用大鼠大脑中动脉缺血2h/再灌注22h模型,神经病学评分,脑梗塞范围及脑组织水含量变化,观察脑康灵胶囊抗脑缺血/再灌注损伤的效应;通过测定大鼠脑组织中一氧化氮合酶(nitric oxide synthase,NOS),超氧化物歧化酶(superoxide disumtase,SOD)活性及丙二醛(malondialdehyde,MDA)含量的变化以探讨药物作用的机制。结果脑康灵胶囊可降低大鼠脑缺血/再灌注后神经病学评分及梗塞范围,降低脑组织MDA,NOS含量及升高SOD活性。结论脑康灵胶囊对脑缺血/再灌注损伤有保护作用,其作用机制与抑制NOS活性、抗脂质过氧化、提高SOD活性有关。     

康脑神注射液对大鼠脑缺血再灌注损伤的防治作用研究

目的研究康脑神注射液对大鼠脑缺血再灌注损伤的保护作用。方法采用双侧颈总动脉结扎法建立大鼠脑缺血再灌注模型,观察脑组织含水量及脑组织匀浆中Na 及Ca2 、兴奋性氨基酸(EAA)、脂质过氧化产物丙二醛(MDA)的动态变化及康脑神注射液对上述指标的影响。结果康脑神注射液可明显降低缺血再灌注大鼠脑组织含水量、脑组织内Ca2 、EAA及MDA含量(P<0.05或0.01)。结论康脑神注射液有抑制大鼠脑缺血再灌注损伤作用,其机制可能与其抑制脑组织内Ca2 及EAA含量、抑制脂质过氧化作用有关。     

益脑胶囊抗衰老作用的实验研究

目的观察益脑胶囊抗衰老的作用。方法建立大鼠急性不完全性脑缺血模型,测定脑组织中超氧化物歧化酶(SOD)、过氧化脂质(LPO)和伊文思蓝的含量,测定正常大鼠血清中SOD的含量。利用大鼠体外颈总动脉-颈外静脉血流旁路法形成血小板血栓,称量血栓湿重。结果益脑胶囊能提高急性不完全性脑缺血模型大鼠脑组织中SOD和伊文思蓝的含量,降低LPO含量,提高正常大鼠血清SOD的含量,抑制大鼠实验性血栓形成。结论益脑胶囊具有预防老年性血管疾病的发生、延缓机体衰老的作用。     

没食子酸十二烷醇酯对大鼠脑缺血再灌注损伤的保护作用

目的：研究没食子酸十二烷醇酯对脑缺血再灌注所致脂质过氧化损伤的保护作用。方法：采用结扎双侧颈总动脉及迷走神经方法,造成大鼠脑缺血90min,随后再灌注45min。结果：没食子酸十二烷醇酯能不同程度地降低脑缺血再灌注大鼠脑组织含水量和MDA含量,提高SOD、CAT和GSP－Px活必,保护Na^ -K^ -ATP酶活性。结论：没食子酸十二烷醇酯可通过保护脑组织抗氧化酶的活性,抑制脂质过氧化反应,减轻自由基对脑组织的损害,对缺血再灌注脑组织产生保护作用。     

康肺神注射液对大鼠脑缺血再灌注损伤的防治作用研究

目的：研究康脑神注射液对大鼠脑缺血再灌注损伤的保护作用。方法：采用双侧颈总动脉结扎法建立大鼠脑缺血再灌注模型，观察脑组织含水量及脑组织匀浆中Na^2 及Ca^2 ，兴奋性氨基酸（EAA），脂质过氧化产物丙二醛（MDA）的动态变化及康脑神注射液对上述指标的影响。结果：康脑神注央求认可明显降低缺血再灌注大鼠脑组织含水量，脑组织内Ca^2 、EAA及MDA含量（P＜0．05或0．01）。结论：康脑神注射液有抑制大鼠脑缺血再灌注损伤的作用，其机制可能与其抑制脑组织内Ca^2 及EAA含量，抑制脂质过氧化作用有关。     

通窍活血汤对脑缺血大鼠的保护作用及机制研究

目的研究通窍活血汤对脑缺血大鼠的保护作用及其机制.方法采用大鼠颈总动脉注入混合血栓诱导剂(ADP、凝血酶、肾上腺素)所致脑血栓模型及脑血栓加双侧颈总动脉结扎所致脑缺血模型,观察通窍活血汤抗脑血栓作用、脑缺血后脑组织的含水量、脑指数及脑组织中的 MDA、SOD 含量的变化.结果通窍活血汤对混合血栓诱导剂所致脑血栓有抑制作用,并能降低脑缺血大鼠脑组织含水量、脑指数,降低MDA的含量,提高SOD的活性.结论通窍活血汤具有较显著的脑缺血保护作用,其作用机制初步认为与抗脑血栓形成、减轻脑水肿、抑制脂质过氧化反应、减轻自由基对脑组织损伤及改善脑缺血后脑组织的病理学损伤等环节有关.     

银杏叶提取物对糖尿病大鼠脂质过氧化作用的影响

目的 研究银杏叶提取物(EGb)抗糖尿病大鼠心肌、睾丸、脑组织脂质过氧化作用。方法 用链脲佐菌素制备SD大鼠糖尿病模型。测定EGb对糖尿病大鼠血液葡萄糖、胰岛素水平,心肌、睾丸、脑组织内超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量的影响。结果 与糖尿病组相比,EGb治疗组大鼠血糖下降、胰岛素升高,心肌、睾丸、脑组织内SOD活性明显升高,MDA含量明显降低。结论 EGb能提高糖尿病大鼠组织抗氧化能力。     

银杏叶提取物EGb761抗大鼠脑缺血损伤的作用机制研究

目的 通过实验研究P38/MAPK和MEK/ERK在大鼠大脑中动脉栓塞模型中的变化及其与EGB761发挥药理作用的关系,探讨银杏叶制剂EGb761治疗脑缺血的机制.方法 大鼠连续1Od口服EGb761 50、100mg/kg后建立大脑中动脉栓塞-再灌模型,通过TTC染色,免疫组化和Westem blot方法检测大鼠脑组织细胞的形态变化和大鼠皮质Caspase -9,Caspase-3,P38/MAPK,MEK/ERK相应蛋白的表达变化.结果 EGb761给药可以减少脑缺血大鼠脑组织梗死面积,显著性抑制脑缺血大鼠海马Caspase-9和Caspase-3表达,显著性抑制大鼠海马神经细胞P-P38,P-MEK和P-ERK的表达水平.结论 EGb761可以减轻脑缺血缺氧引起的细胞损伤,其神经保护作用通过抑制内源性凋亡信号通路激活和P38/MAPK和MEK/ERK信号通路激活引起的细胞凋亡有关.     

3,4-二氯苯丙烯酰另丁胺抗脂质过氧化作用与对大鼠脑缺血的保护作用

 目的：研究3,4-二氯苯丙烯酰另丁胺（简称AED₈₈₀₁）对大鼠脑缺血／再灌注损伤的作用及探讨其在抗脂质过氧化方面的影响。方法：建立Pulsineli四血管阻断大鼠脑缺血／再灌注模型,通过生化检测手段,对脑组织中与脂质过氧化有关的一些指标进行检测。结果：AED₈₈₀₁能使脑缺血／再灌注大鼠脑组织中超氧化物歧化酶（SOD）活性、谷胱甘肽过氧化物酶（Se-GSH-Px）活性增加;脑组织及血清中丙二醛（MDA）含量降低;脑组织中肌酸激酶（CK）、乳酸脱氢酶（LDH）活性提高。结论：AED₈₈₀₁对脑缺血／再灌注损伤具有保护作用,其作用机制可能与其具有抗脂质过氧化作用有关。     

古尼拟青霉对大鼠急性缺血性脑损伤的保护作用及机制研究

 目的研究古尼拟青霉对大鼠急性缺血性脑损伤是否具有保护作用,并探讨其相关机制。方法采用4-动脉阻断法（4-VO）复制大鼠全脑急性缺血30min／再灌注30 min模型。大鼠随机分为假手术组、模型组、古尼拟青霉高、低剂量组和复方丹参组。于造模前连续ig给药3周,再灌注30 min后处死大鼠测定脑组织多项生化指标和观察脑海马CA-1区锥体细胞超微病变。结果与模型组比较,古尼拟青霉高、低剂量组均可增加大鼠脑缺血／再灌注大鼠脑组织中肌酸激酶(CK)和超氧化物歧化酶(SOD)的活性,降低脑组织中丙二醛(MDA)的含量;高剂量组还能增加脑组织中谷胱甘肽过氧化物酶(GSH-Px)的活性、降低脑组织水及Ca^2＋含量,并显著改善海马CA₁区锥体细胞的超微病变。结论古尼拟青霉对大鼠急性全脑缺血／再灌注损伤有一定保护作用,其机制可能与提高脑组织中抗氧化酶活性、减轻脑组织生物膜脂质过氧化损伤及拮抗脑细胞内Ca^{2＋超载有关。}     

The effect of ginkgo biloba extract (EGb 761) pretreatment on intestinal epithelial apoptosis induced by intestinal ischemia/reperfusion in rats: role of ceramide

Apoptosis was demonstrated to be a major mode of intestinal epithelial cell death caused by intestinal ischemia/reperfusion (II/R). Ceramide has been proposed as a messenger for apoptosis. The present study was aimed to investigate the effect of Ginkgo biloba extract 761 (EGb 761) pretreatment on II/R-induced intestinal mucosal epithelial apoptosis in rats and the mechanism related to ceramide. The rat model of II/R injury was produced by clamping superior mesenteric artery for 60 min followed by reperfusion for 180 min. Twenty four rats were randomly allocated into Sham, II/R and EGb + II/R groups. In EGb + II/R group, EGb 761 (100 mg/kg per day) was administered intragastrically for 7 days before the surgery. Animals in II/R and sham groups were treated with equal volume of normal saline solution. Intestinal mucosal epithelial apoptosis was detected via electron microscopy and TUNEL method. Lipid peroxidation in intestinal mucosa was determined by detecting the malondialdehyde level and the activities of superoxide dismutase and peroxidase glutathione. The ceramide generation and sphingomyelinase (SMase) mRNA expression in intestinal mucosa were determined by high performance, thin layer chromatography, and RT-PCR, respectively. II/R caused intestinal mucosal epithelial apoptosis and over-production of the ceramide accompanied by up-regulation of SMase mRNA expression and increases of lipid peroxidation. EGb 761 pretreatment significantly decreased apoptosis index, and concurrently reduced the ceramide generation accompanied by down-regulation of SMase expression and inhibition of lipid peroxidation. The findings indicate that EGb 761 pretreatment attenuates II/R-induced intestinal epithelial apoptosis, which might be attributable to its antioxidant action of mediating ceramide pathway.     

Connexin 43在银杏叶提取物抗大鼠脑缺血损伤中的作用

目的通过体内体外实验研究缝隙连接蛋白43(Cx43)与EGb761脑缺血神经保护作用的关系,探讨银杏叶制剂EGb761治疗脑缺血的机制。方法在大鼠原代神经细胞中转染荷载Cx43-shRNA的慢病毒,干扰Cx43蛋白表达,同时给予EGb761 200μg/mL处理观察Cx43的表达以及EGb761对Cx43蛋白表达的影响。建立大鼠脑缺血模型,腹腔给予EGb761 50、100 mg/kg,使用HE染色,TTC染色,免疫组化和westernblot方法检测大鼠脑组织细胞的形态变化和大鼠海马Caspase-3,TUNEL阳性细胞,Cx43,p-Cx43蛋白的表达变化。结果 EGb761给药可以减少脑缺血大鼠脑组织梗死面积,显著性抑制脑缺血大鼠海马Caspase-3表达和TUNEL阳性凋亡细胞数目,显著性抑制大鼠海马神经细胞p-Cx43的表达水平。体外培养的大鼠神经细胞转染Cx43-shRNA慢病毒,给予EGb761处理,处理前后神经细胞Cx43/p-Cx43蛋白表达未见明显变化。结论 EGb761可以减轻脑缺血缺氧引起的细胞损伤,其神经保护作用与抑制缺血引起的缝隙连接蛋白Cx43的表达和激活有关。     

The effect of Ginkgo biloba extract (EGb 761) on hepatic sinusoidal endothelial cells and hepatic microcirculation in CCl4 rats

It has been shown that Ginkgo biloba Extract (EGb 761) increases peripheral and cerebral blood flow and microcirculation and improves myocardial ischemia reperfusion injury. This study was designed to investigate the effect of EGb 761 on hepatic endothelial cells and hepatic microcirculation. Sixty male Wister rats were divided into normal, carbon tetrachloride (CCl4) and EGb groups, and were given normal saline, CCl4 and CCl4 plus EGb 761, respectively, for 10 weeks. Samples were taken from the medial lobe of the rat livers ten weeks later. Hepatic sinusoidal endothelial cells and other parameters of hepatic microcirculation were observed under transmission electron microscopy (TEM). The amount of malondialdehyde (MDA), endothelin (ET-1), platelet-activating factor (PAF) and nitric oxide (NO) in liver tissue was determined by spectrophotometry and radioimmunoassay, respectively. Compared with the CCl4 group, aggregation of blood cell or micro thrombosis in hepatic sinusoids, deposition of collagen in hepatic sinusoids and space of Disse, injury of endothelial cells and capillization of hepatic sinusoid was significantly reduced in the EGb group. The amount of MDA, ET-1 and PAF was markedly reduced in the EGb group than in the CCl4 group, while no significant difference in the amount of NO was observed between the two groups. The results demonstrate that EGb 761 has protective effect on hepatic endothelial cells and hepatic microcirculation in rats with chronic liver injury induced by CCl4. The mechanisms may involve its inhibition on ET-1, PAF and lipid peroxidation.     

康脑液对脑缺血再灌注损伤大鼠血清及脑组织匀浆SOD、MDA、NO的影响

目的观察康脑液对脑缺血再灌注损伤大鼠血清及脑组织匀浆超氧化物歧化酶（SOD）、丙二醛（MDA）及一氧化氮（NO）含量的影响。方法将大鼠随机分为分为假手术组、模型组及康脑液干预组。康脑液干预组每日以康脑液灌胃,假手术组以生理盐水灌胃,连续15 d后,用颈动脉引流法复制脑缺血模型,分别测定各组血清、脑组织匀浆中SOD、MDA及NO的含量。结果康脑液能显著降低脑缺血再灌注损伤大鼠血清及脑组织中MDA及NO的含量,提高SOD的活性。结论康脑液对脑缺血再灌注损伤有一定的预防和保护作用,机制与抗自由基、抑制脂质过氧化反应等有关。     

The Ginkgo biloba extract, EGb 761, fails to reduce brain infarct size in rats after transient, middle cerebral artery occlusion in conditions of unprevented, ischemia-induced fever

There is much biochemical evidence, but very few studies in animal models of stroke in vivo, to suggest that Ginkgo biloba (EGb 761) may offer neuroprotection against regional, ischemic brain damage; additional investigations are needed to ensure future clinical trials. This study reports the effects of EGb 761 given acutely or chronically before ischemia. Rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h and the brain infarct size was assessed 24 h later. Dipyrone (100 mg/kg, i.p.) was injected 30 min before ischemia, and 2.5 and 5.5 h after ischemia, to reduce ischemia-induced fever. EGb 761 (Tebonin) was given acutely (200 mg/kg, p.o., 60 min before ischemia) or chronically (100 mg/kg, p.o., once daily, for 14 days before ischemia). Acute or chronic treatment with EGb 761, either alone or in combination with dipyrone, did not reduce the infarct size compared with saline alone (p > 0.05). Dipyrone failed to prevent ischemia-induced fever during the intra-ischemic period (p > 0.05 vs saline; p < 0.001 vs sham). In the reperfusion phase, dipyrone reduced fever to normothermic levels in the group treated acutely with EGb 761 (p < 0.01 vs saline, p > 0.05 vs sham) but not after chronic EGb 761 (p < 0.01 vs sham), indicating possible pharmacokinetic interaction. In conclusion, within the context of unprevented, ischemia-induced fever, the present results demonstrate that EGb 761 has no significant effect on brain infarct size.     

Gingko biloba extract inhibits oxidative stress and ameliorates impaired glial fibrillary acidic protein expression, but can not improve spatial learning in offspring from hyperhomocysteinemic rat dams

We aimed to study the effects of gingko biloba extract (EGb) on oxidative stress, astrocyte maturation and cognitive disfunction in offspring of hyperhomocysteinemic rats. Hyperhomocysteinemia was induced in the pregnant rats by administration of methionine (1 gr/kg body weight) dissolved in drinking water throughout pregnancy. One group of animals has received same amount of methionine plus 100 mg/kg/day EGb during pregnancy. On the postnatal day 1, half of the pups from all groups were sacrificed to study the lipid peroxidation (LPO) in different subfractions of brain. Other half of pups were tested in Morris water maze to assess differences in learning and memory performance at the 75 days of age. Maternal hyperhomocysteinemia significantly increased LPO levels especially in mitochondrial subfraction of fetal pup brains. EGb significantly prevented this LPO inrease. Methionine administration to animals reduced glial fibrillary acidic protein (GFAP) expression in pup brains significantly. EGb administration improved GFAP expression significantly. Offspring of hyperhomocysteinemic animals had poor long term spatial memory performance on Morris water maze and EGb administration had no effect on impaired spatial memory. In conclusion, maternally induced hyperhomocysteinemia significantly increased oxidative stress, decreased expression of GFAP and impaired learning performance. Copyright © 2011 John Wiley & Sons, Ltd.