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1.
炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),病因和发病机制尚不清楚。肠黏膜局部免疫反应异常是UC发病的重要环节。炎症介质[包括活性氧簇(ROS)和细胞因子]在介导这一异常免疫反应中起重要作用。本研究观察银杏天宝(Ginkgo biloba extract,EGB)对2,4,6-三硝基苯磺酸(TNBS)诱导实验性结肠炎大鼠炎症介质的影响,探讨银杏天宝对大鼠实验性结肠炎的影响机制。一、材料和方法1.材料和试剂:TNBS购自Sigma公司。EGB为贵州 相似文献
2.
炎症性肠病的病因和发病机制尚不清楚 ,Rachmilewitz等[1] 发现 ,炎症性肠病活动期患者病变肠段一氧化氮合酶(NOS)活性和一氧化氮 (NO)生成量明显高于正常对照组 ,推测NO可能参与其发病过程。为此 ,我们使用不同剂量的NG 硝基 L 精氨酸甲酯 (NG nitro L argininemethylester,L NAME)抑制NOS活性 ,以探讨NO参与炎症性肠病的可能机制与组织损伤间的关系。材料和方法一、大鼠结肠炎模型的建立和实验分组成年雄性Wistar大鼠 5 0只 ,体重 190~ 2 30 g ,随机取 10只为空白对… 相似文献
3.
清肠栓对溃疡性结肠炎大鼠一氧化氮和一氧化氮合酶活性的影响 总被引:10,自引:0,他引:10
目的:观察不同剂量清肠栓治疗溃疡性结肠(UC)的作用及其对一氧化氮(NO)和一氧化氮合酶(NOS)活性的影响。方法:将动物随机分成高、中、低剂量清肠栓组、SASP组、模型组、空白组,除空白组外其余5组动物分别用三硝基苯磺酸(TNBS)建立大鼠溃疡性结肠炎模型,连续用药2周后取结肠组织,采用改良的G法、分光光度法分别测定其NO含量和NOS活性。结果:模型组大鼠NO、NOS含量较空白组明显降低,其他各组均有不同程度的增高,尤其以清肠栓高剂量组的增高为明显。结论:TNBS急性损伤使结肠组织的NO、NOS活性发生改变,可能是UC发生的重要机制。中药复方清扬栓具有调控NO及NOS活性的作用,是有效治疗UC的可能机制之一。 相似文献
4.
硫酸锌对溃疡性结肠炎治疗作用的实验研究 总被引:4,自引:0,他引:4
目的:建立一种慢性溃疡性结肠炎(Ulcerativecolitis,UC)的动物模型,并在此基础上观察硫酸锌灌肠治疗UC的疗效。方法:Wistar大鼠,给予含1.5%的sodiumdextransulfate水自由饮用,形成大鼠溃疡性结肠炎模型,给予硫酸锌灌肠治疗,内镜检查观察疗效。同时检测了治疗前后结肠粘膜SOD活性、MDA含量和锌含量。结果:硫酸锌灌肠应用治疗UC疗效与地塞米松相仿,治疗后结肠粘膜锌含量、SOD活性增高,MDA含量下降。结论:硫酸锌可用于溃疡性结肠炎的治疗,治疗作用与锌元素的局部对抗氧自由基的损害有关。 相似文献
5.
目的 观察褪黑激素对中老年大鼠脑、肝、肾过氧化脂质产物含量和氧自由基、细胞内钙离子清除能力的影响,探讨其抗氧化作用及机理。方法 边续30d给中老年大鼠补充褪黑激素,采用生化比色等方法,测定脑、肝、肾内丙二醛9MDA)含量和谷胱甘 过氧化物酶(GSH-Px)、氢过氧化物酶9CAT)、钙离子-三磷酸腺甙酶(Ca^2+-ATPae)活性。结果 与对照组比较,实验组大鼠脑、肝、肾、MDA含量有不同程度的下 相似文献
6.
目的探讨肠康颗粒对溃疡性结肠炎大鼠一氧化氮(NO)水平及一氧化氮合酶(NOS)活力的影响。方法 Wistar大鼠60只随机分为乙醇对照组、模型组、肠康饮低、中、高剂量组,柳氮磺吡啶(SASP)组,每组10只。应用2,4,6-三硝基苯磺酸(TNBS)复制溃疡性结肠炎动物模型,21 d后处死大鼠,观察大体形态学及组织病理学改变,并运用硝酸还原法检测各组大鼠NO水平及NOS活力。结果肠康颗粒能有效降低NOS活性及NO水平。结论肠康颗粒对大鼠实验性溃疡性结肠炎疗效显著,可能是通过抑制NOS表达,减少NO生成,从而减轻NO引起的损伤有关。 相似文献
7.
NF-κB、iNOS在大鼠实验性结肠炎肠组织的表达及意义 总被引:2,自引:0,他引:2
目的观察大鼠实验性溃疡性结肠炎肠组织核因子-κB(NF-κB)及iNOS、NO的表达,探讨NF-κ:B在溃疡性结肠炎发病过程中的作用.方法采用三硝基苯磺酸(TNBS)制备大鼠溃疡性结肠炎模型,动物分为正常组、生理盐水组及轻、重模型组共4组.采用免疫组织化学染色检测肠组织NF-κB、iNOS表达,生化方法检测MPO、NO含量,并分析NF-κ:B活性与肠道病理损伤指数、MPO、NO含量及iNOS表达的关系.结果与正常组及生理盐水组相比,溃疡性结肠炎大鼠肠组织中NF-κB活性,iNOS表达及NO含量、MPO活性显著增高(P<0.01),且在病情严重组增高尤为明显.NF-κ:B表达水平与iNOS阳性细胞密度、NO含量、MPO活性及肠道病理损伤指数呈显著正相关关系(P<0.01).结论NF-κ:B、iNOS可能参与了溃疡性结肠炎发生、发展. 相似文献
8.
超氧化物歧化酶脂质体治疗大鼠实验性结肠炎的研究 总被引:1,自引:0,他引:1
溃疡性结肠炎 (UC) ,是病因未明的慢性非特异性肠道炎症性疾病 ,常迁延不愈 ,反复发作 ,严重影响患者的正常工作和生活。因此 ,探索各种治疗方法显得日趋重要。据文献报道 ,重要的炎症介质如氧自由基 (OFR)、一氧化氮 (NO)及其代谢产物过量生成 ,在 UC和实验性结肠炎的发生、发展过程中起着重要作用 [1,2 ]。有学者应用超氧化物歧化酶 (SOD)脂质体治疗 UC和克隆病 (CD) [3,4 ] ,取得了良效 ,但这些研究是非对照性的。本实验进行对照研究 ,观察SOD脂质体对大鼠实验性结肠炎的疗效 ,并同 5 -氨基水杨酸 (5 - ASA)进行对比 ,试图为临… 相似文献
9.
川芎嗪对实验性溃疡性结肠炎治疗作用的研究 总被引:6,自引:0,他引:6
目的:研究川芎嗪对小鼠溃疡性的炎的治疗作用及其机制。方法:在小鼠溃疡性结肠炎模型上观察川芎嗪的治疗作用,并用免疫组化LSAB(labelled streptavidin biotin)法检测肠组织中P选择素的表达,用ELISA法检测血浆P选择素含量。结果:溃疡性结肠炎小鼠结肠粘膜充血、水肿、糜烂或溃疡性形成;粘膜炎症细胞浸润(主要为中性粒细胞)及隐窝脓肿形成;川芎嗪治疗组小鼠未见明显病理变化,疾病活动指数(DAI)和病理学评分明显改善。免疫组化和ELISA检测发现,溃疡性结肠炎时肠组织P选择素表达和血中P选择素水平显著升高,经川芎嗪治疗的小鼠P选择素明显下降。结论:P选择素与溃疡性结肠炎密切相关,川芎嗪对溃疡性结肠炎具有治疗作用。 相似文献
10.
目的 研究雷米普利通过抗氧化作用改善大鼠心衰的作用机制.方法 结扎大鼠左冠状动脉前降支造模成功并饲养6 w的16只存活大鼠随机分为模型组及雷米普利组,每组8只,另随机选9只作为假手术组(麻醉开胸后只穿刺不结扎,1只死于麻醉意外),连续灌胃给药4 w后测定全血黏度,检测血清超氧化物歧化酶(SOD)活性,血清丙二醛(MDA)、脂质过氧化物(LPO)、游离脂肪酸(FFA)含量,并通过HE染色观察梗死区心肌组织形态学变化.结果 雷米普利可明显降低MDA、LPO及FFA含量,提高SOD活性,并能减轻梗死区心肌细胞肥大及间质纤维化.结论 雷米普利改善左室重构的作用机制可能与其增强抗氧化酶活性,减少自由基对心肌的氧化损伤有关. 相似文献
11.
目的探讨银杏叶提取物(EGB)对实验性结肠炎大鼠肠组织大体形态组织学及炎性指标的影响。方法利用三硝基苯磺酸灌肠制备大鼠实验性结肠炎模型。实验设正常对照组、模型组、5-氨基水杨酸组、EGB组。4周后评价结肠组织大体形态和组织学评分,检测髓过氧化物酶(MPO)活性和IL-6、IL-6 mRNA表达。结果模型组大鼠结肠组织大体形态和组织学评分较对照组显著增加,MPO活性、IL-6、IL-6 mRNA表达水平显著升高;EGB组上述指标较模型组显著下降。结论EGB对大鼠实验性结肠炎有一定治疗作用,其作用机制可能与其降低结肠组织细胞因子IL-6水平有关。 相似文献
12.
目的研究冠心病病人血浆氧自由基与一氧化氮(NO)及纤溶活性的关系及银杏叶提取物的抗损伤作用。方法观察30例正常人及92例冠心病(稳定性心绞痛、不稳定性心绞痛、陈旧性心肌梗塞)病人血浆丙二醛(MDA)、超氧化物歧化酶(SOD)、NO、组织纤溶酶原激活物(t-PA)、t-PA抑制物(PAI)变化;并观察66例冠心病病人口服银杏叶提取物(天保宁)15天后上述指标的改变。结果三组冠心病人血浆MDA、PAI均显著高于正常人,SOD、t-PA、NO均显著低于正常人。病人服天保宁15天后可明显减少血浆中MDA、PAI,升高SOD、t-PA、NO水平。结论冠心病病人血浆氧自由基较正常人明显增高,并可引起血管内皮细胞损伤,NO合成减少,纤溶活性下降;而天保宁具有抗氧化损伤作用,增加NO合成,改善纤溶功能。 相似文献
13.
银杏叶提取物及其合剂对饲胆固醇兔动脉粥样硬化的作用 总被引:5,自引:0,他引:5
目的:研究银杏叶提取物和银杏叶提取物合剂(银杏叶提取物+维生素E+L-精氨酸+牛磺酸,2:1:2:2.5)对饲胆固醇兔动脉粥样硬化的防治作用。方法采用饲1%胆固醇兔形成动脉粥样硬化为模型,观察银杏叶提取物和银杏叶提取物合剂对饲胆固醇兔胸主动脉动脉粥样硬化斑块面积百分比及对血浆丙二醛和一氧化氮含量的影响。结果银杏叶提取物合剂(1-3mg/kgperday)和银杏叶提取物(0.5mg/kgperday 相似文献
14.
银杏叶提取物对大鼠应激性溃疡的保护作用 总被引:11,自引:4,他引:7
目的 探讨银杏叶提取物(EGb) 对大鼠应激性胃溃疡发生的保护作用.方法 ♂ Wistar 大鼠,随机分成对照组、模型组和EGb 处理组;通过胃窦部埋置电极记录束缚水浸应激过程胃平滑肌电活动变化,同时测定血浆和胃粘膜组织中丙二醛( MDA) 水平及观察胃粘膜的病理改变情况.结果 应激模型组大鼠胃电活动节律明显紊乱、慢波振幅和峰电位发放率较对照组显著增加,MDA 显著升高( P< 0-05) ,并伴有胃粘膜广泛充血、溃疡;EGb 15 m g/ kg 腹腔注射预处理可显著压抑( P< 0-01) 应激过程的胃电紊乱、降低 MDA 水平和胃粘膜溃疡指数.结论 EGb 对束缚水浸应激引起的胃运动功能障碍和胃粘膜溃疡有明显地保护作用,其机制可能是通过调整平滑肌电活动和对自由基的清除. 相似文献
15.
Summary Effects of preconditioning and Ginkgo biloba extract (EGb 761) were studied in isolated non-diabetic and diabetic ischaemic
and re-perfused rat hearts. Hearts were randomly divided into five groups in both the age-matched non-diabetic and the 8-week
streptozotocin-induced diabetic groups: Group I, hearts were subjected to 30 min of global ischaemia followed by 30 min of
re-perfusion; Group II, one cycle of preconditioning consisting of 5 min ischaemia and 10 min re-perfusion before the induction
of 30 min of ischaemia and 30 min of re-perfusion; Group III, two cycles of preconditioning; Group IV, three cycles; and Group
V, four cycles before the onset of 30 min ischaemia followed by 30 min of re-perfusion. Four cycles of ischaemic preconditioning
resulted in a reduction of arrhythmias in non-diabetic rats. Thus, in non-diabetics, the incidence of ventricular fibrillation
and tachycardia fell from 92 % and 100 % (no preconditioning) to 33 % (p < 0.05) and 42 % (p < 0.05), respectively. Four cycles of preconditioning failed to reduce the incidence of re-perfusion arrhythmias in diabetic
subjects. Preconditioning reduced the formation of oxygen free radicals measured by electron spin resonance spectroscopy,
but the recovery of cardiac function was low in all non-diabetic and diabetic preconditioned groups. EGb 761 at 25 and 50
mg/kg improved cardiac function in non-preconditioned and preconditioned non-diabetic and diabetic hearts. During re-perfusion
in the four-cycle preconditioned non-diabetic and diabetic groups, the amount of free radicals was reduced approximately by
50 and 70 % using 25 and 50 mg/kg of EGb 761, respectively. EGb 761 improved cardiac function after ischaemia in both non-preconditioned
and preconditioned non-diabetic and diabetic rats. Our data suggest that diabetes could abolish the precondition-induced protection.
[Diabetologia (1996) 39: 1255–1262]
Received: 28 March 1996 and in revised form: 3 June 1996 相似文献
16.
Protective effects of Ginkgo biloba extract on the ethanol-induced gastric ulcer in rats 总被引:3,自引:0,他引:3
Chen SH Liang YC Chao JC Tsai LH Chang CC Wang CC Pan S 《World journal of gastroenterology : WJG》2005,11(24):3746-3750
AIM: To evaluate the preventive effect of Ginkgo biloba extract (GbE) on ethanol-induced gastric mucosal injuries in rats. METHODS: Female Wistar albino rats were used for the studies. We randomly divided the rats for each study into five subgroups: normal control, experimental control, and three experimental groups. The gastric ulcers were induced by instilling 1 mL 50% ethanol into the stomach. We gave GbE 8.75,17.5,26.25 mg/kg intravenously to the experimental groups respectively 30 min prior to the ulcerative challenge. We removed the stomachs 45 min later. The gastric ulcers, gastric mucus and the content of non-protein sulfhydryl groups (NP-SH), malondialdehyde (MDA), c-Jun kinase (JNK) activity in gastric mucosa were evaluated. The amount of gastric juice and its acidity were also measured. RESULTS: The findings of our study are as follows: (1) GbE pretreatment was found to provide a dose-dependent protection against the ethanol-induced gastric ulcers in rats; (2) the GbE pretreatment afforded a dose-dependent inhibition of ethanol-induced depletion of stomach wall mucus, NP-SH contents and increase in the lipid peroxidation (increase MDA) in gastric tissue; (3) gastric ulcer induced by ethanol produced an increase in JNK activity in gastric mucosa which also significantly inhibited by pretreatment with GbE; and (4) GbE alone had no inhibitory effect on gastric secretion in pylorus-ligated rats. CONCLUSION: The finding of this study showed that GbE significantly inhibited the ethanol-induced gastric lesions in rats. We suggest that the preventive effect of GbE may be mediated through: (1) inhibition of lipid peroxidation; (2) preservation of gastric mucus and NP-SH; and (3) blockade of cell apoptosis. 相似文献
17.
银杏叶提取物与秋水仙碱对大鼠肝纤维化预防作用的比较 总被引:2,自引:0,他引:2
目的比较银杏叶提取物(GBE)和秋水仙碱对实验性大鼠肝纤维化的预防作用。方法SD雄性大鼠40只随机分为4组:正常组(n=10)、模型组(n=10)、秋水仙碱预防组(n=10)及GBE预防组(n=10)。模型组、秋水仙碱预防组及GBE预防组给予500 mL/L CCl4腹腔注射,1 mL/kg,每周2次,共8周,秋水仙碱预防组每天同时给予秋水仙碱灌胃,0.2 mg/kg,GBE预防组每天同时给予GBE灌胃,0.3 g/kg。实验结束后,心脏取血分离血清行肝功能生化指标检测,处死动物取肝脏甲醛固定,常规行HE染色,免疫组化检测α-SMA和TGF-β1。结果光镜下组织学检查纤维化分级GBE预防组低于秋水仙碱预防组(P0.05),肝功能生化指标检测GBE预防组优于秋水仙碱预防组[ALT:(168.4±34.6)U/Lvs(210.6±40.8)U/L;AST:(318.8±62.5)U/Lvs(511.2±53.2)U/L;ALB:(31.0±2.1)g/Lvs(28.1±2.0)g/L;P均0.05],免疫组化检测α-SMA及TGF-β1蛋白表达GBE预防组低于秋水仙碱预防组(α-SMA:29.3±1.5vs5.1±2.2;TGF-β1:14.5±0.9vs28.6±0.9)。结论GBE预防大鼠肝纤维化的作用优于秋水仙碱,GBE作为一种新的抗肝纤维化药物有很好的研究和应用前景。 相似文献
18.
19.
Xiao Yun JIANG Li Ping QIAN Xiao Juan ZHENG Yu Ye XIA Yi Bin JIANG Da Yu SUN 《Journal of digestive diseases》2009,10(4):293-299
OBJECTIVE: To investigate the effect of Ginkgo biloba extract on gastric precancerous lesions in rats. METHODS: 80 4‐week‐old Wistar rats were randomly divided into four groups: a control group, a model group, a low and a high dose Ginkgo biloba extract intervention group; 20 in each group. Gastric precancerous lesions were induced by giving them 100 mg/L N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) solution to drink ad libitum for 20 weeks. In addition to the MNNG, the intervention groups were lavaged with Ginkgo biloba extract (0.5 mg/kg/d in the low dose group, 1.5 mg/kg/d in the high dose group) for 20 weeks. Starting from week 21 all the rats were fed with normal rat chow and tap water. At the end of week 30 the rats were killed. The histopathological changes of their gastric mucosa, ISA, NGI, the serum and gastric mucosal SOD/MDA and the expressions of oncogenes were studied. RESULTS: The incidence of mild to severe intestinal metaplasia and dysplasia were significantly lower in the intervention groups than those in the model group (P < 0.01). The ISA and NGI in the intervention groups were significantly lower than those in the model group (P < 0.01). In the intervention groups the activity of SOD was increased and the concentration of MDA was decreased (P < 0.01). Expressions of Bcl‐2, c‐myc and FasL decreased in the intevention groups, whereas the expression of Fas increased. When compared with the model group, the differences were statistically significant (P < 0.01, P < 0.05, respectively). CONCLUSION: Ginkgo biloba extract can increase anti‐oxidative activity and inhibit the progression of gastric precancerous lesions via the regulation of cell proliferation and apoptosis. 相似文献
20.
目的:建立紫外线C辐射(UV-C)在SD大鼠体内诱导产生氧化应激的模型,并观察银杏提取物GBE50(Ginkgo biloba extract 50)对其保护及治疗作用。方法:采用253.7nm紫外灯进行辐照,连续7d,每天2h,辐照密度2.381mW/(cm2·h),每日辐射量为18W/cm2,建立UV-C在SD大鼠体内诱导产生氧化应激的模型,通过对各脏器组织还原型谷胱甘肽水平、超氧化物歧化酶(SOD)活性以及丙二醛水平进行检测,评价标准治疗量[100mg/(kg·d)]的GBE50的保护及治疗作用。结果:GBE50对UV-C辐射诱导的氧化应激模型有一定的保护治疗作用,可以提高肝脏、心脏和脑组织中SOD活性和肝脏及脑组织中谷胱甘肽还原酶活性,并降低心脏和脑组织中丙二醛水平。结论:GBE50应用于氧化应激的保护具有良好前景。 相似文献