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1.
目的 研究低氧条件下Rho激酶是否参与低氧引起的血管平滑肌细胞增生。方法 组织块法培养大鼠肺动脉平滑肌细胞(PASMCs)。应用甲基噻唑基四唑(MTT)比色法观察细胞增生情况;流式细胞仪观察细胞周期的变化;蛋白质免疫印迹法(Western blot)检测Rho激酶的表达。结果 缺氧组MTT比色吸光度(A)值显著高于常氧组.缺氧24h+Rho激酶抑制剂Y27632组A值显著低于缺氧24h组;缺氧组细胞周期G2/M期细胞比例显著高于常氧24h组,缺氧24h+Y27632组细胞比例显著低于缺氧24h组。Western blot结果表明各缺氧组Rho激酶表达均明显高于常氧组,其中以缺氧24h组表达增高最明显;Rho激酶在缺氧24h+Y27632组明显低于缺氧24h组。结论 缺氧可诱导PASMCs增殖,缺氧诱导的增生PASMCs中Rho激酶活性水平增加,提示缺氧致PASMCs增殖过程中Rho激酶可能发挥重要作用。  相似文献   

2.
Rho激酶是具有GTP酶活性蛋白Rho下游的一个重要效应分子,在肌动蛋白细胞骨架重构和细胞收缩、黏附、迁移、增殖和凋亡方面起重要作用。随着Rho激酶抑制剂法舒地尔和Y27632的发现,Rho激酶的生物学功能得到广泛关注。Rho/Rho激酶信号通路参与多种肺部疾病的发生、发展,在这些疾病的动物模型中阻断该信号通路可改善疾病的病理变化和预后。本文就Rho激酶及Rho激酶抑制剂在肺部疾病中的作用研究进展作一综述。  相似文献   

3.
目的通过在体外用Rho相关卷曲螺旋形成的蛋白激酶(ROCK)特异性抑制剂Y-27632处理人食管癌细胞株TE13,观察Y-27632对TE13的生长及迁移能力的影响,并探讨其可能机制。方法体外培养人食管癌株TE13,分别用不同浓度的Y-27632(2.5、5、10、20μmol/L)处理细胞24 h,对照组加等体积PBS,采用细胞计数、MTT检测细胞生长情况,采用划痕实验观察细胞的迁移能力,采用Western blot检测小窝蛋白(cav)-1的表达水平。结果 Y-27632可以促进细胞的生长与迁移能力,随着时间的增加促进效果越明显,与对照组比较存在明显差异(P<0.05)。Y-27632可以上调cav-1表达水平。结论 ROCK信号通路参与TE13细胞生长与迁移的调节,Y-27632可以增加TE13细胞的生长及迁移能力,其机制可能与上调cav-1的表达有关。  相似文献   

4.
目的研究ROCK特异性抑制剂Y-27632对人食管癌EC9706细胞迁移能力的影响,并探讨其可能的机制。方法体外培养人食管癌株EC9706,加入20μmol/L的Y-27632溶液(实验组)及等体积的PBS(对照组)培养1 h,采用细胞计数、MTT实验检测细胞生长情况,采用Transwell实验观察细胞迁移情况,采用Western blot检测Cav-1的表达水平,并进行两组的比较。结果细胞计数、MTT、Transwell实验结果显示,Y-27632可以抑制细胞的生长与迁移能力,与对照组比较差异有统计学意义(P均<0.05)。Western blot检测结果显示,Y-27632处理细胞1 h后,Cav-1蛋白表达水平明显下降,并明显低于对照组(P均<0.05)。结论 ROCK信号通路参与EC9706细胞生长与迁移的调节,Y-27632可以抑制EC9706细胞的生长及迁移能力,其机制可能与下调Cav-1的表达有关。  相似文献   

5.
背景:Rho激酶抑制剂可以调节细胞骨架重构,激活转录因子,促进细胞增殖和分化。目的:观察Rho激酶抑制剂Y-27632对大鼠骨髓间充质干细胞分裂增殖和细胞周期的影响。方法:采用贴壁细胞培养法体外分离培养SD大鼠骨髓间充质干细胞,并传代。取生长状态良好的第2代骨髓间充质干细胞分组:实验组加入10μmol/LRho激酶抑制剂Y-27632,对照组正常培养。结果与结论:①骨髓间充质干细胞增殖:细胞生长曲线呈"S"型,Rho激酶抑制剂Y-27632作用后,3d左右进入平台期,细胞生长加速,生长曲线上移。②骨髓间充质干细胞的细胞周期:对照组G0/G1期细胞比例为(80.640±5.516)%,S期细胞比例为(13.397±2.511)%;实验组G0/G1期细胞比例为(61.723±8.829)%,S期细胞比例为(29.380±7.630)%,实验组S期细胞比例高于对照组(P<0.05)。表明Rho激酶抑制剂Y-27632可以促进骨髓间充质干细胞DNA的合成,促进细胞分裂和增殖。  相似文献   

6.
目的:探讨Rho激酶抑制剂法舒地尔对慢性低灌注大鼠认知功能损害的影响及其可能机制。方法:60只雄性Wistar大鼠随机分为假手术组、缺血组、法舒地尔组各20只,缺血组及法舒地尔组结扎双侧颈总动脉,而假手术组不结扎;术后假手术组和缺血组每日腹腔注射生理盐水1mL,法舒地尔组每日腹腔注射法舒地尔2mg/kg。于术后第23天开始对大鼠进行为期5d的水迷宫适应训练,术后第28、29天评测大鼠认知功能,术后第30天将大鼠处死取脑,采用RTPCR测定Rho激酶mRNA表达水平,并采用组织化学染色观察海马一氧化氮合酶(NOS)阳性神经元的形态和数目。结果:与假手术组比较,缺血组大鼠认知功能显著降低,Rho激酶mRNA表达水平明显增高,海马NOS阳性神经元数目增多且染色较深;与缺血组比较,法舒地尔组大鼠认知功能改善,海马N0s阳性神经元数目减少且染色变浅,但Rho激酶mRNA表达水平无明显差异。结论:慢性低灌注大鼠认知功能明显降低,Rho激酶异常活化与一氧化氮产生增多可能参与其作用机制;Rho激酶抑制剂法舒地尔可改善慢性低灌注大鼠的认知损害,其作用机制并非调控Rho激酶的基因表达,可能与改善脑血流、抗过氧化应激作用有关。  相似文献   

7.
目的:观察Rho A相关细胞骨架调控信号通路在慢性坐骨神经结扎(chronic sciatic nerve constriction injury,CCI)神经病理性疼痛大鼠背根神经节激活及辛伐他汀(simvastatin)鞘内给药对该通路影响。方法:42只质量180~200 g SD雄性大鼠随机分为5组:Na?ve组(n=6)、Sham组(n=6)、CCI组(n=18)、Simvastatin组(n=6)及Rho激酶(Rho kinase,ROCK)抑制剂Y-27632组(n=6)。对大鼠行鞘内置管,于造模后7天结扎CCI组、Simvastatin组及Y-27632组大鼠单侧坐骨神经构建CCI模型,术后Simvastatin组每天鞘内注射10μl辛伐他汀(10μg/μl),Y-27632组每天鞘内注射12μl Y-27632(4 mg/ml),Na?ve组、Sham组、CCI组术后每天鞘内注射生理盐水10μl,连续注射7天。于CCI建模后1、3、7、14天进行动物行为学评估,观察大鼠对机械和热刺激的反应。于建模后第14天处死大鼠,取手术侧L4~6背根神经节(dorsal root ganglion,DRG),并进行实时定量PCR观察RhoA、ROCK的m RNA表达变化,免疫荧光观察Rho A蛋白在DRG伤害性神经元中的分布及改变,以及免疫荧光强度随建模时间梯度增加,Western blot检测通路中主要因子RhoA、LIMK和cofilin蛋白水平表达的改变。结果:1 Simvastatin组大鼠给予辛伐他汀后第3天起缩足反射热辐射潜伏期、缩足反射机械刺激阈值明显高于CCI组,差异具有统计学意义(P<0.05);ROCK抑制剂Y-27632组大鼠缩足反射热辐射潜伏期、缩足反射机械刺激阈值给药后3天起较CCI组明显提高,差异具有统计学意义(P<0.05)。2 CCI组大鼠DRG中Rho A、ROCK m RNA于术后第7天起表达显著增加(P<0.05);Rho A蛋白在背根神经节神经元中表达,CCI术后14天Rho A免疫荧光强度与Na?ve组比显著增高(P<0.05)。3鞘内注射辛伐他汀能显著抑制通路主要因子Rho A、p-LIMK、p-cofilin的表达(P<0.05)。结论:大鼠CCI慢性神经病理性疼痛存在Rho A/LIMK/cofilin通路的激活,辛伐他汀鞘内注射可抑制该通路的活化,为治疗神经病理性疼痛提供新的靶点。  相似文献   

8.
背景:Rho及其相关分子在神经轴突生长、分化、延伸及突触形成中起重要作用,阻断和抑制RhoA/ROCK通路可促进神经干细胞的增殖与生长。目的:观察Rho激酶抑制剂法舒地尔和RNAi介导的RhoA基因沉默对大鼠神经干细胞增殖的影响。方法:体外培养Wistar胎鼠神经干细胞,分6组干预:空白对照组,5,10,15,20μmol/L法舒地尔组,siRNA沉默RhoA基因组。干预后第3天,采用RT-PCR,Westernblot检测各组神经干细胞RhoA基因及蛋白的表达。应用MTT比色法观察神经干细胞增殖情况;采用流式细胞术测定神经干细胞周期分布的变化。结果与结论:15,20μmol/L法舒地尔组、siRNA沉默RhoA基因组神经干细胞RhoA基因及蛋白表达量较5,10μmol/L法舒地尔组、空白对照组明显降低(P〈0.05),细胞的生长速度较5,10μmol/L法舒地尔组、空白对照组明显增快(P〈0.05),细胞周期G0/G1期减少(P〈0.05),S期细胞数增多(P〈0.05)。当法舒地尔浓度增加到20μmol/L时对细胞的作用并非随浓度的增加而增强,与15μmol/L组的差异无显著性意义(P〉0.05)。15,20μmol/L法舒地尔组与siRNA沉默RhoA基因组相比差异无显著性意义(P〉0.05)。说明Rho激酶抑制剂法舒地尔和RNAi介导的RhoA基因沉默在体外均能促进神经干细胞增殖,法舒地尔最佳作用浓度为15μmol/L。  相似文献   

9.
陈庆奇  董少红 《临床荟萃》2012,27(18):1568-1570,1574,F0002
目的探讨Rho激酶抑制剂对血管平滑肌细胞核因子κB的作用,为动脉粥样硬化的治疗提供新的思路。方法体外培养大鼠主动脉平滑肌细胞,传代3~5代后给予抗平滑肌细胞特异性蛋白α-肌动蛋白(α-SMC)进行鉴定;分为空白对照组、血管紧张素Ⅱ(Ang-Ⅱ)组及白细胞介素1(IL-1)组,其中Ang-Ⅱ组及IL-1组又分为直接刺激组及Rho激酶抑制剂Y-27632干预组,分别按组别给予相应的药物干预,然后提取核蛋白,再行化学发光法(EMSA)检测核因子-κB(NF-κB)的表达。结果对照组血管平滑肌细胞未检出NF-κB活性,给予Ang-Ⅱ及IL-1β刺激后,NF-κB活性明显增高。在加用Y27632预处理后再给予Ang-Ⅱ及IL-1β刺激,NF-κB活性较直接刺激组有下降。条带密度分析显示,给予Ang-Ⅱ及IL-1β刺激后,NF-κB活性的相对密度值为1.31±0.21和1.09±0.07,加用Y27632预处理后再给予Ang-Ⅱ及IL-1β刺激,条带相对密度值分别为0.58±0.23和0.54±0.11,较直接刺激组有明显下降(P<0.05或<0.01)。结论 Ang-Ⅱ及IL-1具有刺激NF-κB表达的作用,Rho激酶抑制剂Y-27632能下调上述的刺激作用,并可能通过此机制起到抗动脉粥样硬化的作用。  相似文献   

10.
背景:前期实验表明增生性瘢痕中RhoA和ROCK-I基因表达较正常皮肤高,提示RheA/ROCK-I信号通路可能参与了增生性瘢痕的发生,但其在病理性瘢痕中的作用尚不清楚.目的:研究RhoA/ROCK-I信号通路在增生性瘢痕成纤维细胞结缔组织生长因子(connective tissue growth factor,CTGF)表达调控中的作用.方法:分离培养人增生性瘢痕组织来源的成纤维细胞,应用转化生长因子β1及Rho激酶的特异抑制剂Y-27632对细胞进行干预实验.采用实时荧光定量PCR及免疫荧光细胞化学方法检测瘢痕成纤维细胞中RhoA,ROCK-I及CTGF mRNA与蛋白的表达.结果与结论:给予转化生长因子β1后,增生性瘢痕成纤维细胞中RheA,ROCK-I及CTGF mRNA与蛋白表达明显增多(P<0.01):而Y-27632能阻碍转化生长因子β1的作用;但单独给予Y-27632并不引起瘢痕成纤维细胞中RhoA,ROCK-I及CTGF的mRNA与蛋白表达改变.说明转化生长因子β1可通过RhoA/ROCK-I信号通路调控CTGF mRNA与蛋白的表达,即RhoA/ROCK-I信号通路参与了瘢痕成纤维细胞CTGF的表达调控,阻断RheA下游通路是增生性瘢痕治疗靶点之一.  相似文献   

11.
目的:探讨细胞周期抑制剂Roscovitine(Ros)对糖氧剥夺(OGD)诱导的鼠大脑皮质神经元凋亡的保护作用及可能机制。方法:体外培养大鼠皮质神经元,随机分为对照组、OGD1h后恢复糖氧供给(OGD/R)3h、6h、12h、24h组及Ros(100μM)组。Western Blot检测各组神经元磷酸化视网膜母细胞瘤蛋白(p-Rb)和E2F1的表达情况;免疫荧光细胞化学染色观察OGD/R12h组及Ros组神经元p-Rb表达;TUNEL法检测OGD/R12h组及Ros组神经元凋亡情况。结果:OGD/R各组神经元p-Rb及E2F1的表达均较对照组增高(P<0.05),12h达最高;Ros组p-Rb及E2F1的表达减少,少于OGD/R12h组(P<0.05);Ros组p-Rb和TUNEL阳性细胞率均低于OGD/R 12h组(P<0.01),两组中大部分TUNEL阳性细胞与p-Rb表达共定位。结论:Ros可能通过抑制Rb磷酸化及E2F1介导的凋亡机制来减少缺血缺氧后的神经元凋亡。  相似文献   

12.
背景:在神经细胞培养中实验性缺氧缺糖在一定程度上模拟缺血性卒中,对于研究缺血性神经元损伤的进程和病理生理学机制有非常重要的用处.目的:在神经元培养时制作实验性缺氧缺糖模型.设计、时间及地点:分组对照观察,实验于2007-01/2008-03在北京大学第三医院中心实验室完成. 材料:17-19 d胎龄的Wistar大鼠.方法:细胞培养取17~19 d胎龄的Wistar大鼠的皮质神经元做原代细胞培养,并且去掉污染的非神经原细胞.缺氧缺糖的诱导分为3组:实验组将第7天的皮质神经元置于无糖甲衡盐溶液和2%去氧酶中,在37℃的潮湿保温箱中培育.空白对照组培养基为含20 mmol/L葡萄糖的无去氧酶平衡盐溶液.假性实验组培养基为含20 mmol/L葡萄糖和失活的去氧酶平衡盐溶液.主要观察指标:以血气分析进行氧浓度的测定;以相差显微镜观察实验组培养细胞神经元死亡状况;以用乳酸脱氢酶检测盒检测乳酸脱氢酶活性;以锥虫蓝染色观察缺氧缺糖对神经元存活力的影响.结果:氧浓度测定显示在加入去氧酶后培养基迅速产生缺氧状态;乳酸脱氢酶检测显示在用去氧酶和无糖平衡盐处理后,培养基中乳酸脱氢酶释放显著增加;锥虫蓝染色和相差显微镜检查显示经去氧酶和无糖平衡盐处理后实验组的细胞活力明显下降,大部分神经元在6 h死亡.结论:实验结果显示去氧酶与无精平衡盐液可联合用于神经元培养时产生缺氧缺糖状态,其在体外模拟脑缺血的相关研究中有重要作用.  相似文献   

13.
目的:胎鼠原代皮层神经元培养,建立N-甲基-D-天冬氨酸(NMDA)诱导的兴奋性毒性损伤模型。研究丹红注射液对于神经元NMDA损伤后的保护作用。方法:胎鼠原代神经元培养并鉴定。培养至10d时,给予不同浓度NMDA,采用MTT法检测细胞生存率并测定LDH释放率,建立NMDA损伤模型。给予两种剂量的丹红注射液干预,测定细胞生存率及LDH释放率。采用Hoechst染色及TUNEL检测小剂量丹红干预组细胞凋亡情况。结果:随着NMDA浓度的增高,神经元生存率逐步下降,LDH释放率依次增加,以NMDA300μmol·L^-1组损伤最明显。丹红干预组细胞生存率提高,LDH释放率下降。小剂量丹红干预组凋亡细胞百分率减低。结论:丹红注射液可减轻NMDA诱导的体外神经元损伤,抑制神经元凋亡。  相似文献   

14.
Cyclooxygenase isozymes (COX-1 and COX-2) are found to be constitutively expressed in brain, with neuronal expression of COX-2 being rapidly induced after numerous insults, including cerebral ischemia. Because overactivation of N-methyl-D-aspartate (NMDA) receptors has been implicated in the cell loss associated with ischemia, we characterized the expression of the COX isozymes in murine mixed cortical cell cultures and used isozyme-selective inhibitors to determine their relative contribution to NMDA receptor-stimulated prostaglandin (PG) production and excitotoxic neuronal cell death. Immunocytochemical analysis of mixed cortical cell cultures revealed that COX-2 expression was restricted to neurons, whereas COX-1 was expressed in both neurons and astrocytes. Brief exposure to NMDA (5 min; 100 microM) elicited a time-dependent accumulation of PGs in the culture medium that preceded neuronal cell death and correlated with the induction of COX-2 mRNA. COX-1 expression remained unchanged. Flurbiprofen, a nonselective COX-1/COX-2 inhibitor, blocked NMDA-stimulated PG production and attenuated neuronal death in a concentration-dependent manner. Similar results were obtained with the specific COX-2 inhibitor NS-398 (10-30 microM) but not with the selective COX-1 inhibitor valeryl salicylate (10-300 microM). Inhibition of total constitutive COX activity with aspirin (100 microM, 1.5 h) before NMDA exposure did not prevent subsequent NMDA-mediated neuronal cell death. However, neuronal injury in aspirin-pretreated cultures was attenuated by flurbiprofen administration after NMDA exposure. Finally, the protection afforded by COX-2 inhibition was specific for NMDA because neither flurbiprofen nor NS-398 protected neurons against kainate-mediated neurotoxicity. Together, these results support the conclusion that newly synthesized COX-2 protein contributes to NMDA-induced neuronal injury.  相似文献   

15.
The ability of several glutamate receptor antagonists to reduce hypoxic cortical neuronal injury was quantitatively examined in cell cultures derived from fetal mice. Cultures exposed to hypoxia for 8 hr showed by the following day widespread neuronal injury, which was substantially attenuated by addition of the specific N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonovalerate (APV). The protective effect of APV was concentration dependent (ED50 about 2 microM) and stereospecific (D-APV approximately 100 times more potent that L-APV). Neuron-protective effects were also observed with several other NMDA antagonists: 2-amino-7-phosphonoheptanoate, phencyclidine and (+)-SKF 10,047 [(+)-N-allylnormetazocine]--as well as with the nonspecific glutamate antagonists D-glutamylglycine and kynurenate. In addition, a similar antagonist profile was observed with a chemical model of hypoxic neuronal injury, produced by brief exposure to high concentrations of cyanide. In contrast, 1 mM concentrations of glutamate diethylester and gamma-aminomethyl sulfonate, compounds reported in some studies to preferentially antagonize non-NMDA glutamate receptors, failed to protect neurons against either hypoxia or cyanide. These results are consistent with the hypothesis that NMDA receptors are preferentially involved in the pathogenesis of hypoxic cortical neuronal injury and suggest that cortical cell culture may be a useful system in which to quantitatively characterize the pharmacology of that injury.  相似文献   

16.
We recently described a screening system designed to detect neurotoxicity of artemisinin derivatives based on primary neuronal brain stem cell cultures (G. Schmuck and R. K. Haynes, Neurotoxicity Res. 2:37-49, 2000). Here, we probe possible mechanisms of this brain stem-specific neurodegeneration, in which artemisinin-sensitive neuronal brain stem cell cultures are compared with nonsensitive cultures (cortical neurons, astrocytes). Effects on the cytoskeleton of brain stem cell cultures, but not that of cortical cell cultures, were visible after 7 days. However, after a recovery period of 7 days, this effect also became visible in cortical cells and more severe in brain stem cell cultures. Neurodegeneration appears to be induced by effects on intracellular targets such as the cytoskeleton, modulation of the energy status by mitochondrial or metabolic defects, oxidative stress or excitotoxic events. Artemisinin reduces intracellular ATP levels and the potential of the inner mitochondrial membrane below the cytotoxic concentration range in all three cell cultures, with these effects being most dominant in the brain stem cultures. Surprisingly, there were substantial effects on cortical neurons after 7 days and on astrocytes after 1 day. Artemisinin additionally induces oxidative stress, as observed as an increase of reactive oxygen species and of lipid peroxidation in both neuronal cell types. Interestingly, an induction of expression of AOE was only seen in astrocytes. Here, manganese superoxide dismutase (MnSOD) expression was increased more than 3-fold and catalase expression was increased more than 1.5-fold. In brain stem neurons, MnSOD expression was dose dependently decreased. Copper-zinc superoxide dismutase and glutathione peroxidase, two other antioxidant enzymes that were investigated, did not show any changes in their mRNA expression in all three cell types after exposure to artemisinin.  相似文献   

17.
Stem cell factor stimulates neurogenesis in vitro and in vivo   总被引:35,自引:0,他引:35       下载免费PDF全文
Cerebral ischemia stimulates neurogenesis in proliferative zones of the rodent forebrain. To identify the signaling factors involved, cerebral cortical cultures prepared from embryonic mouse brains were deprived of oxygen. Hypoxia increased bromodeoxyuridine (BrdU) incorporation into cells that expressed proliferation markers and immature neuronal markers and that lacked evidence of DNA damage or caspase-3 activation. Hypoxia-conditioned medium and stem cell factor (SCF), which was present in hypoxia-conditioned medium at increased levels, also stimulated BrdU incorporation into normoxic cultures. The SCF receptor, c-kit, was expressed in neuronal cultures and in neuroproliferative zones of the adult rat brain, and in vivo administration of SCF increased BrdU labeling of immature neurons in these regions. Cerebral hypoxia and ischemia may stimulate neurogenesis through trophic factors, including SCF.  相似文献   

18.
Spinal cord injury (SCI) often leads to persistent functional deficits due to loss of neurons and glia and to limited axonal regeneration after injury. Here we report that transplantation of human dental pulp stem cells into the completely transected adult rat spinal cord resulted in marked recovery of hind limb locomotor functions. Transplantation of human bone marrow stromal cells or skin-derived fibroblasts led to substantially less recovery of locomotor function. The human dental pulp stem cells exhibited three major neuroregenerative activities. First, they inhibited the SCI-induced apoptosis of neurons, astrocytes, and oligodendrocytes, which improved the preservation of neuronal filaments and myelin sheaths. Second, they promoted the regeneration of transected axons by directly inhibiting multiple axon growth inhibitors, including chondroitin sulfate proteoglycan and myelin-associated glycoprotein, via paracrine mechanisms. Last, they replaced lost cells by differentiating into mature oligodendrocytes under the extreme conditions of SCI. Our data demonstrate that tooth-derived stem cells may provide therapeutic benefits for treating SCI through both cell-autonomous and paracrine neuroregenerative activities.  相似文献   

19.
纳洛酮对缺氧大鼠皮层神经元细胞的保护作用   总被引:10,自引:1,他引:9  
目的 观察缺氧对大鼠皮层神经元细胞的影响及纳洛酮的保护作用。方法 取体外培养 12d的Wistar大鼠皮层控经元细胞 ,随机分为正常对照组、缺氧组、纳洛酮组 (缺氧前 2 4h加纳洛酮预处理 ) ;缺氧 6h后在常氧下继续培养 2 4h。观察各种条件下神经元细胞的存活率和形态学的改变 ,测定培养液中乳酸脱氢酶 (LDH)含量。结果 缺氧后可见神经元胞体肿胀、细胞死亡 ,LDH渗出量增多 ,细胞存活率减少 (P <0 0 1)。经纳洛酮预处理的神经元 ,缺氧后神经元胞体肿胀、细胞死亡程度轻于缺氧组 ,LDH渗出显著低于缺氧组 (P <0 0 1) ,而存活率明显高于缺氧组 (P <0 0 1)。结论 缺氧能诱导皮层神经元损伤 ,而纳洛酮对神经元的缺氧损伤具有明显的保护作用  相似文献   

20.
背景纳洛酮对脑缺血再灌注损伤细胞的保护作用机制尚不明确.选择体外培养皮质神经元研究纳洛酮疗效可排除多重因素干扰.目的观察缺氧对体外培养大鼠皮质神经元的影响及纳洛酮的保护机制.设计重复测量设计.地点和对象实验地点军事医学科学院神经生物学研究室.研究对象体外培养12 d的Wistar大鼠皮质神经元.干预取体外培养12 d的Wistar大鼠皮质神经元,随机分为正常对照组、缺氧组、纳洛酮组(缺氧前24 h加纳洛酮预处理);缺氧6 h后在常氧下继续培养24 h.主要观察指标观察各种条件下神经元的存活率和形态学的改变,测定培养液中乳酸脱氢酶(LDH)含量.结果缺氧后可见神经元胞体肿胀、细胞死亡,LDH渗出量增多[6 h正常对照组为(78.68±7.34)%,缺氧组为(194.38 ±22.32)%;12 h正常对照组为(77.98±8.85)%,缺氧组为(331.66±36.12)%],细胞存活率减少[6 h正常对照组为(91.82±2.89)%,缺氧组为(66.96±4.98)%;12 h正常对照组为(90.84±2.61)%,缺氧组为(32.02±6.34)%],差异有显著性意义(P<0.01).经纳洛酮预处理的神经元,缺氧后神经元胞体肿胀、细胞死亡程度轻于缺氧组,LDH渗出[6 h(159.86±34.03)%;12 h(256.28±28.29)%]显著低于缺氧组(P<0.01),而存活率[6 h(78.08±4.15)%;12 h(53.68±4.32)%]明显高于缺氧组,差异有显著性意义(P<0.01).结论对缺氧诱导的皮质神经元的损伤,纳洛酮具有明显的保护作用.  相似文献   

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