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1.
纳洛酮对大鼠局灶性脑缺血再灌注损伤的保护作用   总被引:4,自引:0,他引:4  
目的 观察纳洛酮对大鼠局灶性脑缺血再灌注损伤的保护作用。方法 用改良Longa法制作局灶性脑缺血再灌注损伤模型 ,观察不同剂量纳洛酮对模型大鼠神经功能障碍、脑梗死范围、脑组织病理改变以及血清中乳酸脱氢酶(LDH)和肌酸激酶 (CK)含量的影响。结果 纳洛酮能剂量依赖性地降低模型大鼠的血清LDH、CK ,减少梗死面积 ,降低神经功能行为评分 ,减轻脑组织病理改变。结论 纳洛酮对大鼠局灶性脑缺血再灌注损伤有一定的保护作用  相似文献   

2.
利用细胞凋亡抑制基因bcl-2单克隆抗体及免疫组化LSAB法,对正常外阴皮肤、慢性外阴营养不良、不典型增生和外阴癌组织进行标记,发现bcl-2蛋白在正常外阴皮肤基底层中有弱阳性表达;在增生型营养不良、不典型增生及外阴癌组织中表达率有不同程度增高,与外阴硬化苔癣型和混合型营养不良有显著差异(P<0.05,P<0.05,P<0.01);而增生型与不典型增生bcl-2基因蛋白表达无明显差异(P>0.05);外阴癌的表达率最高;该基因蛋白表达与外阴癌细胞分化程度有关,与临床分期无关。  相似文献   

3.
目的研究七叶皂苷钠(sodium β-aescin)对大鼠局灶性脑缺血再灌注后基质金属蛋白酶-9(matrix metallopro-teinase-9,MMP-9)和层黏连蛋白(laminin,LN)表达影响,为深入探讨七叶皂苷钠对脑的保护机制提供实验依据。方法制备大鼠局灶性脑缺血再灌注模型,随机分为正常组、假手术组、缺血再灌注组和缺血再灌注七叶皂苷钠治疗组,后两组又分为缺血2h后再灌注3、6、12、24、72h和7d,共6个时间点,每时间点4只;用免疫组织化学法和图像分析观察其缺血区LN和MMP-9的表达变化。结果缺血再灌组MMP-9在神经元的表达于再灌注6h开始增加,12h达高峰,24h又降低,7d最低,治疗组MMP-9于再灌注同一时相有显著减少;LN在微血管的表达于再灌注12h明显减少,24h时达低峰,72h开始回升,治疗组在同一时相LN表达显著增多。结论MMP-9与LN可能参与脑血管源性脑水肿的形成发展,缺血再灌注早期七叶皂苷钠治疗通过减少MMP-9的表达,增加LN的表达对缺血再灌注脑起保护作用。  相似文献   

4.
应用图像分析仪对60例乳癌bcl-2、PCNA和雌孕激素受体进行免疫组织化学及酶联亲和法定量研究。结果表明:bcl-2蛋白定量高值组,乳癌组织学分级低,患者生存期长、生存率高(P<0.05);PCNA表达定量高值组,组织学分级高,患者生存期短、生存率低(P<0.05)。显示了定量检测bcl-2蛋白和PCNA对评估乳癌分化程度及判断预后具有一定价值。bcl-2与雌孕激素受体间有显著的正相关性(P<0.001),提示bcl-2蛋白检测对乳癌患者内分泌治疗有重要参考价值。  相似文献   

5.
目的探讨姜黄素对沙土鼠脑缺血再灌注后凋亡相关基因Bcl-2、Bax在海马CA1区、CA3区表达的影响及意义。方法制作沙土鼠双侧颈总动脉阻断缺血再灌注损伤模型。随机分为假手术组(SH).脑缺血再灌注组(IR)、姜黄素组(CU)、对照组(SC),每组据再灌注时间点不同又分为1、3、5、7d4个亚组,每组6只动物。在预定时间点行开阔法行为学检查,TUNEL法检测海马CA1区、CA3区细胞凋亡,免疫组织化学染色测定Bcl-2、Bax蛋白在海马CA1区、CA3区的表达变化。结果姜黄素可显著减少沙土鼠探索活动及海马CA1、CA3区凋亡锥体细胞数量(与IR组相比,P〈0.01),诱导Bcl-2蛋白及抑制Bax蛋白表达(与IR组相比,P〈0.01)。结论姜黄素有脑保护作用,调控凋亡相关基因Bcl-2、Bax蛋白的表达可能是其作用机制之一。  相似文献   

6.
目的探讨姜黄素对沙土鼠脑缺血再灌注后凋亡相关基因Bcl-2、Bax在海马CA1区、CA3区表达的影响及意义。方法制作沙土鼠双侧颈总动脉阻断缺血再灌注损伤模型。随机分为假手术组(SH)、脑缺血再灌注组(IR)、姜黄素组(CU)、对照组(SC),每组据再灌注时间点不同又分为1、3、57、d 4个亚组,每组6只动物。在预定时间点行开阔法行为学检查,TUNEL法检测海马CA1区、CA3区细胞凋亡,免疫组织化学染色测定Bcl-2、Bax蛋白在海马CA1区、CA3区的表达变化。结果姜黄素可显著减少沙土鼠探索活动及海马CA1、CA3区凋亡锥体细胞数量(与IR组相比,P<0.01),诱导Bcl-2蛋白及抑制Bax蛋白表达(与IR组相比,P<0.01)。结论姜黄素有脑保护作用,调控凋亡相关基因Bcl-2、Bax蛋白的表达可能是其作用机制之一。  相似文献   

7.
本文应用链霉新合素-生物素-过氧化物酶技术,P185的特殊抗体,旨在检测40例良恶性涎腺肿瘤标本中是否有P185的过量表达,以及探讨其与临床病理指标之间是否存在着相关关系。  相似文献   

8.
目的研究褪黑素对脑缺血再灌注后Nrf2/HO-1信号通路的调控作用。方法 SPF级雄性SD大鼠99只随机分为假手术组、脑缺血再灌注组、褪黑素处理组,对脑缺血再灌注组和褪黑素处理组采用线栓法制作脑缺血再灌注模型,缺血90 min后拔出线栓进行再灌注,褪黑素处理组在再灌注即刻和12 h后按5 mg/kg体质量腹腔注射褪黑素,脑缺血再灌注组腹腔注射3.43 mol/L无水乙醇生理盐水溶液;改良Garcia JH评分评估3组动物神经缺损的严重程度,Nissle染色观察24 h后梗死面积,HE染色观察3组大鼠脑组织梗死灶神经元的改变,免疫组化观察3组大鼠组间HO-1、GFAP和NF200的表达情况,Western blot检测3组大鼠组间Nrf2和HO-1的表达。结果褪黑素处理能提高脑缺血再灌注后1、3、7 d神经功能评分(P<0.05);褪黑素处理后可以增加脑缺血急性期Nrf2和HO-1的表达(P<0.05);褪黑素处理能减少GFAP的表达(P<0.05),增加NF200的表达。结论褪黑素对脑缺血再灌注损伤有保护作用,其机制可能为褪黑素激活了Nrf2/HO-1信号途径,促进抗氧化蛋白HO-1的表达;同时,褪黑素可能抑制神经胶质细胞生成胶质瘢痕,有利于神经轴突再生。  相似文献   

9.
目的研究全脑缺血再灌注损伤后JUN蛋白在大鼠海马的表达及热休克预处理对其表达的影响。方法以四血管法建立全脑缺血再灌注模型。将大鼠置于42℃中15 min行热休克预处理,全脑缺血6 min后行2 h、6 h、12 h、24 h3、d、5 d再灌注后处死,取海马脑组织行HE染色、JUN蛋白免疫组化染色,TUNEL法检测凋亡细胞。结果缺血再灌注后2 h JUN蛋白在CA1区开始表达,6 h达到高峰,5 d时仍有表达;CA3区JUN蛋白的表达弱于CA1区(P<0.05);同时CA1区细胞损伤明显。热休克预处理组JUN蛋白表达在CA1和CA3区相应时点减弱(P<0.05),细胞损伤轻微,凋亡细胞减少(P<0.05)。结论全脑缺血再灌注损伤后JUN蛋白过度表达参与了神经元损伤过程,热休克预处理通过下调JUN蛋白过度表达具有脑保护作用。  相似文献   

10.
应用免疫组化SP法对32 例早期胃癌及癌旁粘膜和24 例慢性萎缩性胃炎中bcl 2 的表达同时进行检测,结果癌旁和慢性萎缩性胃炎中不典型增生、单纯增生、腺体扩张和癌旁肠化均显示bcl 2 高表达,与癌无显著差异( P> 005),应视作癌前病变。bcl 2 在癌前病变和早期胃癌中的表达显著高于周围正常粘膜( P<001),提示bcl 2 高表达是胃癌发生的早期事件,在胃癌发生上起着重要作用,可作为胃癌早期诊断的可靠指标  相似文献   

11.
Thesequenceofeventsthroughwhichischaemialeadstocelldeathispoorlyunderstood.Anumberofendogenouscomponentshavebeenimplicatedinthesubsequentneurodegenerativeprocess,suchasglutamate,freeradicals,calciumandpolyamines,allofwhichhavebeenshowedtobeelevatedinassociationwithischaemicinsults.Agentssuchasglutamineandcalciumhaveestablishedrapidandpotentphysiologicalactions,thatareexaggeratedduringischaemia,leadingtoamassiveanduncontrolledamplificationoftheirnormaleffects.Animportantcomponentofthephysiologi…  相似文献   

12.
Objective Ependymal cells are thought to be the primary source of neural stem cells in the adult central nervous system. The purpose of this study is to examine spatial and temporal profiles of ependymal cell proliferation and migration after focal cerebral ischemia. Methods Eighty male Sprague Dawley rats underwent permanent middle cerebral artery occlusion after injection of 10/μL of 0.2% Dil into the lateral ventricle. Rats were sacrificed and brain sections were acquired for pathological evaluation and laser confocal imaging at day 1,3,7,11,14,21 and 28 after ischemia. Results The density of Dil-labeled cells in the ischemic ipsilateral subventricular zone was significantly higher than that in the control group and these labeled cells dispersed in the ischemic ipsilateral subventricular zone and/or were located in ependyma from day 1 to 11. In the ischemic ipsilateral cortex, some Diilabeled cells occurred in peri-infarction and infarction of parietal region at day14 and peaked at day 21 when some Dil-labeled cell nodules were found in this region. During postischemic day 14--28, a significant decrease in labeled celldensity in the ischemic ipsilateral subventricular zone was coincident with a significant increase in labeled cells density in the cortex (peri-infarction and infarction). Conclusion The results indicate that ependymal cells proliferate and migrate after focal cerebral ischemia in the adult rat brain.  相似文献   

13.
Objective To explore the effect of Ligustrazine on neurogenesis in cortex after focal cerebral ischemia in rats. Methods Focal cerebral ischemia was induced by left middle cerebral artery occlusion with a suture. Two hours later, injection of Ligustrazine (80 mg/kg, 1 time/d) was performed peritoneally. Four hours after the ischemia, 5-bromodeoxyuridine (BrdU) (50 mg/kg, 1 time/d) was injected peritoneally. At 7 d, 14 d and 21 d after ischemia, BrdU positive cells in the cortex were observed by cal staining. Results In ischemic model group, at 7 day, sparsely-distributed BrdU positive cells were observed in the Ⅱ-- Ⅵ layers of the ipsilateral cortex, with a bandlike distribution in ischemic penumbra. With the prolongation of ischemia, the number of BrdU positive cells increased. In Ligustrazine group, BrdU positive cells were also observed in theⅡ-- Ⅵ layers of the cortex, with an intense distribution in ischemic penumbra. The numbers of BrdU positive cells at 7 d, 14 d and 21 d were more than those in ischemic model group respectively. Conclusion Ligustrazine increases the proliferated cells in cortex after focal cerebral ischemia in rats. The results suggest that it may be useful for promoting self-repair after ischemia.  相似文献   

14.
用复方中药给家兔灌饲7d后,分别测兔脑缺血30min及再灌流60min、120min时脑组织中LPO舍量、SOD活力;另给“血瘀”家兔模型灌饲该中药7d后测血液流变学变化。结果:该中药能显著降低脑缺血后再灌流120min时脑组织LPO含量、保护SOD活力、降低全血粘度、抑制ADP诱导的血小板聚集,提示该中药可保护兔脑缺血性损伤。作用机理:①抗氧自由基损伤;②通过降低血浆纤维蛋白原含量降低全血粘度。  相似文献   

15.
16.
Objective To study the expression of interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R), determine the alteration of erythrocytic immunity and T cell subgroup in the blood of outer circulation in patients with hypertensive cerebral hemorrhage so and to probe into the relationship between them, and to explore the clinical significance. Methods Enzyme linked immnunosorbent assay (ELISA) was used to determine the content of IL-2 and slL-2R. The immunoadsorption was employed to examine the erythrocytic immune activity and its regulating function. ( S-P) was used to determine the cell number of CD3 (cluster of differentiation3), CD4 and CD8. Resolts The content of IL-2 in the group with hypertensive cerebral hemorrhage was significantly lower than that in the control group (P〈0.01), and the content of sIL-2R increased. Red blood cell C3b receptor (RBC. C3bR) and RBC immune adherence enhancing factor (RFEB) dropped greatly (P〈0.01), while RBC immune complex rosette (RBC. ICR) and RBC immune adherence inhibiting factor (RFIR) increased greatly. The cell number of CD3 and CD4decreased (P〈0.01) and there was no obvious change in CD8 (P〈 0. 05). Conclusion The decrease of immune function was observed in patients with hypertensive cerebral hemorrhage. The determination of the content of IL-2, sIL- 2R, erythrocytic immunity and the activity of T subgroup has an important clinical significance in the occurrence, development, treatment, and prognosis of hypertensive cerebral hemorrhage.  相似文献   

17.
Adenosine (Ado) is an endogenous purine nu-cleoside that slows the sinus heart rate (negativechronotropic effect) as well as impulse conductionthrough the atrioventricular (AV) node (negativedromotropic effect )[1.2J. Two subtypes of adeno-sine receptors (A,, A,) have been identified basedon biochemical and radioligand binding studies inthe heart and pharmacology responses to Ado andadenosine derivatives. The predominant antiar-rhythmic effects on the sinoatrial (SA) node, AVnode, and atri…  相似文献   

18.
利用一对玻璃微电极同时记录内外膜下心肌细胞的跨膜电位,研究了模拟缺血再灌注条件下,3,6-[二甲胺基]-二苯骈碘杂六环枸橼酸盐对离体豚鼠心室肌心律失常及跨壁传导等电生理特性的影响。结果显示,其可明显性降低心律失常发生率、改善缺血再灌过程的跨壁传导阻滞、相对增加有效不应期、减少触发活动的发生。  相似文献   

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