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1.
目的 探讨依达拉奉对大鼠局灶性脑缺血再灌注损伤后神经功能损伤、细胞凋亡及caspasc-3蛋白表达的影响.方法 雄性SD大鼠24只采用随机数字表法分为假手术组、脑缺血再灌注组、生理盐水治疗组、依达拉奉治疗组,每组6只.除假手术组外,其余3组均采用大脑中动脉线栓法制作大鼠局灶性脑缺血再灌注损伤模型.依达拉奉治疗组于脑缺血开始时及再灌注后12 h分别腹腔注射依达拉奉3 mg/kg,生理盐水治疗组同时间注射等量生理盐水;假手术组同样过程造模,但不插入尼龙线造成缺血.造模后24 h后进行大鼠神经行为学评分;应用免疫组织化学及Western blot检测caspase-3蛋白表达水平的变化;利用原位缺口末端标记法(TUNEL法)研究神经细胞凋亡的变化.结果 与脑缺血再灌注组及生理盐水治疗组相比,依达拉奉治疗组大鼠神经行为学评分明显减少,caspase-3免疫阳性细胞及蛋白表达明显减少,凋亡细胞也减少,差异均有统计学意义(P<0.05).结论 依达拉奉能有效减轻脑缺血灌注损伤后神经细胞凋亡.改善神经功能缺损症状,推测其机制与抑制caspase-3蛋白表达有关.  相似文献   

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目的探讨自由基清除剂依达拉奉预处理对大鼠脑缺血再灌注损伤后神经细胞凋亡及其相关蛋白Bcl-2、Bax、热休克蛋白70(HSP70)表达的影响。方法将45只雄性SD大鼠随机分为假手术组、对照组、依达拉奉预处理组,每组15只。采用线栓法制作大鼠缺血2h再灌注24h模型。预处理组大鼠建模前12h腹腔注射依达拉奉(3mg/kg),对照组给予等容量生理盐水。再灌注24h后断头取脑,应用免疫组织化学法检测Bcl-2、Bax、HSP70蛋白表达,末端脱氧核糖核酸转移酶介导的原位缺口末端标记法检测凋亡细胞。结果依达拉奉预处理组和对照组大鼠缺血周围脑组织中凋亡细胞和Bcl-2、Bax及HSP70阳性细胞数比假手术组均明显增加(P<0.01);与对照组比较,其凋亡细胞和Bax阳性细胞数均明显减少(P<0.01),而Bcl-2和HSP70阳性细胞数明显增加(P<0.01)。结论细胞凋亡在缺血再灌注损伤中起着重要作用;依达拉奉可能通过上调Bcl-2、HSP70蛋白表达、下调Bax蛋白表达减轻大鼠脑缺血再灌注后的细胞凋亡,增加脑缺血再灌注损伤耐受性,从而起到神经保护作用。  相似文献   

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目的研究大鼠脑缺血再灌注后Fas相关死亡域蛋白(FADD)、caspase-8蛋白的表达及依达拉奉对其的影响。方法用免疫组化法测定缺血2h后再灌注不同时相缺血半暗带FADD、caspase-8蛋白的表达。结果缺血半暗带皮质内FADD、caspase-8蛋白的表达于缺血再灌注后3h明显上升,再灌注12h达高峰(P〈0.01),至再灌后24h明显下降。依达拉奉能显著下调其表达(P〈0.01,P〈0.05)。结论脑缺血再灌注后缺血半暗带FADD、caspase-8蛋白的表达均明显增加,提示二者可能在脑缺血再灌注损伤中发挥重要作用.依达拉奉可能通过抑制其表达而达到脑保护的作用。  相似文献   

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目的探讨亚低温疗法联合依达拉奉对大鼠脑缺血再灌注损伤后的保护作用。方法采用线栓法建立局灶性脑缺血再灌注模型,缺血6h后再灌注,并分为假手术组、模型组、依达拉奉组、亚低温联合依达拉奉组,再灌注24h后进行神经功能缺损评分,采用TTC染色测定脑梗死体积和用免疫组化的方法检测Bax和Bcl-2的阳性细胞数。结果与模型组比较,依达拉奉未能减少脑梗死体积,但能通过下调Bax及上调Bcl-2减少细胞的凋亡,对脑细胞有保护作用;与模型组、依达拉奉组比较,亚低温联合依达拉奉组能通过上调Bcl-2及下调Bax明显降低大鼠神经缺陷评分及减少脑梗死体积。结论亚低温疗法联合依达拉奉对大鼠脑缺血再灌注损伤具有很好的保护作用。  相似文献   

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目的 观察依达拉奉对IL-1β表达的影响,探讨它的保护作用及机制.方法 Wistar雌、雄性大鼠共42只,随机分为假手术组、盐水对照组及依达拉奉用药组,对照组及用药组再进一步分为3h、6h、24h组,根据Koizumi线栓法建立大鼠左侧大脑中动脉缺血再灌注模型(MCAO),用免疫组化方法检测IL-1β表达的变化.结果 鼠脑缺血再灌注后缺血区脑组织 IL-1β含量,假手术组几乎无表达,盐水组IL-1β表达3h开始升高,于6h到高峰,后逐渐下降.用药组IL-1β的含量较盐水组减少(P<0.05).结论 依达拉奉可减少大鼠脑缺血再灌注后IL-1β表达,起到脑保护作用.  相似文献   

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目的 探讨依达拉奉对糖尿病急性脑缺血再灌注大鼠细胞凋亡及缺氧诱导因子表达的影响.方法 选取健康雄性SD大鼠70只,采用腹腔内一次性注入新鲜配制的1%链尿佐菌素(STZ)及线栓法建立糖尿病大鼠大脑中动脉闭塞再灌注模型.随机分成依达拉奉干预脑缺血再灌注组(干预组)30只、非依达拉奉干预脑缺血再灌注组(非干预组)30只、假手术组5只和正常组5只.前两组又分为缺血2h再灌注1h、6h、12h、24h、48h、72h亚组,每亚组5只.用TUNEL法检测细胞凋亡的变化,用免疫组化法检测缺氧诱导因子(HIF-1α)的表达水平.结果 依达拉奉干预组各个时间点脑皮质区凋亡细胞数及缺氧诱导因子表达量均低于非依达拉奉干预组(P<0.05).结论 依达拉奉可明显减少糖尿病急性脑缺血再灌注大鼠脑神经细胞凋亡数,同时可减少缺氧诱导因子的表达.在糖尿病脑缺血再灌注过程中具有明显神经保护作用.  相似文献   

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[摘要]目的 研究依达拉奉对内质网应激相关因子表达及神经细胞凋亡的影响。 方法 使用SD大鼠短暂性MCAO模型,RT-PCR法检测缺血侧顶叶皮层PERK mRNA、CHOP mRNA表达,免疫组化法检测p-PERK、CHOP蛋白表达,TUNEL法检测神经细胞凋亡。结果 PERK mRNA表达与p-PERK蛋白表达均于再灌注后1h达高峰,其后逐渐下降;再灌注1h缺血侧顶叶皮层CHOP mRNA表达增加,于再灌注12h表达达高峰,再灌注1h缺血侧顶叶皮层可见CHOP蛋白表达,再灌注24h表达达高峰;再灌注1h缺血侧梗死灶周围可以观察到凋亡细胞,至再灌注24h达高峰;依达拉奉能下调PERK、CHOP表达,减少神经细胞凋亡。 结论 依达拉奉能下调PERK、CHOP等ERS基因表达,减少神经细胞凋亡,可能通过抑制内质网应激在上游发挥神经保护作用。  相似文献   

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目的探讨依达拉奉预处理对小鼠脑缺血再灌注(IR)损伤后皮质一氧化氮合酶(NOS)表达的影响。方法 48只健康ICR小鼠被分为假手术组、对照组和依达拉奉组。依达拉奉组和对照组分别给予依达拉奉3 mg/(kg.d)和同等体积的生理盐水腹腔注射共7 d,然后建立小鼠IR模型;缺血1 h、再灌注24 h时应用2,3,5-氯化三苯基四氮唑(TTC)染色法测量各组脑梗死体积,应用免疫组化法检测各组小鼠皮质神经元型、、诱导型和内皮型NOS(nNOS、iNOS、eNOS)阳性细胞数。结果与假手术组比较,对照组小鼠皮质nNOS、iNOS和eNOS阳性细胞数明显增多(均P<0.05);与对照组比较,依达拉奉组脑梗死体积明显缩小,皮质nNOS和iNOS阳性细胞数明显减少,eNOS阳性细胞数明显增多(均P<0.05)。结论依达拉奉预处理可以影响IR小鼠皮质nNOS、iNOS和eNOS的表达,发挥神经保护作用。  相似文献   

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目的探讨补阳还五汤和依达拉奉联用对急性脑缺血损伤后神经细胞凋亡及凋亡相关蛋白表达的影响,探讨其可能的脑保护机制。方法将60只小鼠随机分假手术组、模型组、补阳还五汤组、依达拉奉组以及补阳还五汤+依达拉奉组,每组12只。采用改良线栓法制作小鼠大脑中动脉缺血再灌注模型,给予补阳还五汤及依达拉奉药物干预。分别于再灌注后1d和7d,采用TUNEL法观察小鼠脑皮质缺血区神经细胞凋亡率,采用免疫组化方法观察小鼠脑皮质缺血区B淋巴细胞瘤2基因(bcl-2)、bcl-2相关X蛋白(bax)和半胱氨酸蛋白酶3(caspase-3)表达的阳性细胞数。结果与假手术组比较,模型组小鼠脑皮质缺血区凋亡指数升高(P0.01),且bcl-2、bax和caspase-3表达的阳性细胞亦均升高(P0.01);经补阳还五汤和(或)依达拉奉干预后,各药物组小鼠脑组织的凋亡指数及bax和caspase-3阳性细胞均较模型组下降(P0.01),而脑组织bcl-2阳性细胞均较模型组增加(P0.01),且补阳还五汤+依达拉奉联合用药组较单一用药组改变明显(P0.05)。结论补阳还五汤与依达拉奉联用能抑制脑缺血再灌注损伤后脑细胞中促凋亡蛋白bax、caspase-3的表达;促进具有神经元保护作用的bcl-2蛋白的表达,从而抑制神经细胞凋亡,协同发挥脑保护作用。  相似文献   

10.
大鼠局灶性脑缺血再灌注后海马Bcl-2、Bax蛋白的表达   总被引:1,自引:0,他引:1  
目的 探讨大鼠局灶性脑缺血再灌注后Bcl-2、Bax蛋白在海马表达的变化.方法 线栓法制作大鼠局灶性脑缺血再灌注模型,应用免疫组化染色检测Bcl-2、Bax蛋白表达,应用TUNEL法检测海马区细胞凋亡.结果 缺血再灌注2h后海马神经元Bcl-2、Bax蛋白开始表达,Bcl-2蛋白12h达高峰,Bax蛋白12h~24h达高峰,之后开始下降.再灌注2h后海马凋亡细胞开始表达,随着再灌注时间的延长,其表达不断增加.Bcl-2/ Bax的比率在再灌注开始时升高,再灌注12h达高峰,随后开始下降.结论 凋亡是脑缺血再灌注损伤的重要形式之一,Bcl-2/ Bax的改变与缺血再灌注后海马的神经元存亡有关,缺血再灌注可导致海马神经元凋亡.  相似文献   

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For eating-disordered patients with a history of post-traumatic stress, childhood abuse and neglect, and dissociative disorder, eating behavior symptoms may function as a rational response to unmetabolized traumatic experiences. This paper will review trauma-based theory, dissociation, abreactive, and ego-states therapy as they apply to eating disorder patients.  相似文献   

15.
Decades of intervention research have produced a rich body of evidence on the effects of psychotherapies and pharmacotherapies with children and adolescents. Here we summarize and critique that evidence. We review findings bearing on the efficacy of psychosocial treatments and medications under controlled experimental conditions. We also report evidence, where available, on the effectiveness of both classes of treatment with clinically referred youth treated in real-world clinical contexts. In general, the large body of evidence on efficacy contrasts sharply with the small base of evidence on effectiveness. Addressing this gap through an enriched research agenda could contribute importantly to linking scientific inquiry and clinical practice—to the benefit of both ventures. This is one element of a multifaceted agenda for future research and for synthesis of research, which will require the interplay of multiple disciplines related to child and adolescent mental health.  相似文献   

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OBJECTIVE: The population of Oman is a heterogeneous mix of nationalities providing a natural setting for studying the cross-cultural differences in the presence and severity of eating disorders as well as an opportunity for evaluating the performance of measurement instruments for these disorders. METHOD: Disordered eating screening instruments (the Eating Attitude Test and the Bulimic Investigatory Test) were administered to Omani teenagers, non-Omani teenagers, and Omani adults. RESULTS: On the Eating Attitude Test, 33% of Omani teenagers (29.4% females and 36.4% males) and 9% of non-Omani teenagers (7.5% of males and 10.6% females) showed a propensity for anorexic-like behavior. On the Bulimic Investigatory Test, 12.3% of Omani teenagers showed a propensity for binge eating or bulimia (13.7% females and 10.9% males). Among the non-Omani teenagers, 18.4% showed a tendency toward bulimia, with females showing a slightly greater tendency than males. In contrast, barely 2% of Omani adults showed either a presence of or a severity of disorderly behavior with food. CONCLUSION: Omani teenagers scored significantly higher than other ethnic groups and Omani adults. This finding is discussed in the light of emerging evidence from many parts of the world suggesting that cultural transition, compounded by demographic constraints, plays a significant role in abnormal eating attitudes.  相似文献   

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Abstract

For eating-disordered patients with a history of post-traumatic stress, childhood abuse and neglect, and dissociative disorder, eating behavior symptoms may function as a rational response to unmetabolized traumatic experiences. This paper will review trauma-based theory, dissociation, abreactive, and ego-states therapy as they apply to eating disorder patients.  相似文献   

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Recurrent factors contributing to a recovery process from co-occurring mental health and addiction problems mentioned by users and professionals have been analyzed as part of working alliances and helpful relationships. Still, we lack knowledge about how helpful relationships are developed in daily practice. In this article, we focus on the concrete construction of professional helpful relationships. Forty persons in recovery and fifteen professionals were interviewed. The interviews were analyzed according to thematic analysis, resulting in three themes presented as paradoxes (1) My own decision, but with the help of others; (2) The need for structures and going beyond them; and (3) Small trivial things of great importance. Micro-affirmations have a central role in creating helpful relationships by confirming the individuals involved as more than solely users or professionals. More attention and appreciation should be paid to practices involving micro-affirmations.

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F.S. Labella 《Brain research》1981,219(1):166-171
Specific binding of [3H]naloxone to rat brain tissue in vitro was inhibited by the excitant organochlorinated insecticides (OCI), by ether (E) and octanol (OCT), and by the convulsant indoklon (IND) and its anesthetic isomer, isoindoklon (ISO). In the presence of 100 mM NaCl the inhibition of naloxone binding by E, OCT and ISO was greatly potentiated, whereas that by OCI and IND was attenuated. KCl (100 mM) was equally effective as NaCl on the action of anesthetics, but the effect of the excitant drugs was, in contrast to NaCl, unaffected by KCl. Specific binding of [3H]ouabain in the absence of Na, was depressed by anesthetics and enhanced by neuroexcitants. In the presence of NaCl, which by itself inhibits ouabain binding to brain, both anesthetics and excitants enhanced ouabain binding. DDE, a non-insecticidal analog of DDT, and the dimethyl derivative of the OCI, lindane, were inactive in the receptor assays. These observations point to a unique isolated system which responds consistently to anesthetic agents as a class and, in a different way, to neuroexcitant compounds.  相似文献   

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