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1.
在脑缺血病灶中,中心区神经元坏死为主,周围以缺血半暗带凋亡为主,抑制半暗带细胞的凋亡,可以减少细胞的死亡和脑梗死的面积,因此改善半暗带是治疗脑卒中的关键环节.目前发现MAPK分布于整个中枢神经系统中,MEK/ERK信号通路参与细胞生长、发育、细胞抗凋亡等过程,在脑缺血再灌注损伤过程中有MEK/ERK信号通路的参与,MEK/ERK通路通过影响Bcl-2家族成员的活化和表达调控内源性凋亡途径,ERK通过对细胞周期的调控,抑制胶质细胞大量活化和过度增殖,减少了有害因子并改善局部微循环,从而减少神经元的凋亡.可能为脑血管的防治开辟一条新的途径.本文就MEK/ERK信号通路的结构特点与脑缺血再灌注损伤相关作用机制作一综述.  相似文献   

2.
脑缺血再灌注损伤的主要机制是多种因素诱导的神经元凋亡。近些年来,大蒜素以其脂溶性好,可通过血脑屏障,并具有多种生物功效比如被用于抗细菌、病毒和真菌的感染,尤其是其对于脑保护的作用日益受到重视。本文主要对大蒜素抑制脑缺血再灌注诱导的细胞凋亡的作用及其机制方面做一综述。  相似文献   

3.
目的:探究姜黄素后处理是否通过激活SIRT1/FOXO1信号通路抵抗小鼠脑缺血再灌注损伤。方法:小鼠脑缺血30 min,再灌注24 h建立脑缺血再灌注模型。手术前脑室内注射SIRT1特异性抑制剂EX527。再灌注后腹腔注射姜黄素。小鼠随机分为以下6组:假手术组;单纯姜黄素后处理组;缺血再灌注组;缺血再灌注+姜黄素后处理组;EX527预处理+缺血再灌注+姜黄素后处理组;EX527预处理+脑缺血再灌注组。再灌注24 h检测脑梗体积、Complex I活性、ROS含量以及SIRT1、Ac-FOXO1、Bax、Bcl-2、Caspase-3蛋白表达情况。结果:与手术组相比,姜黄素后处理组梗死区脑组织SIRT1的表达量及活性明显增加,脑梗体积降低,ROS含量降低而Complex I活性增高,Bcl-2的表达增高而Bax和Caspase-3的表达量降低(均P0.05)。阻断SIRT1信号通路后上述姜黄素脑保护作用均减弱(P0.05)。结论:我们的研究首次证实姜黄素后处理通过激活SIRT1/FOXO1信号通路,进而降低氧化应激与凋亡,最终减轻脑缺血再灌注损伤。  相似文献   

4.
脑是人体对缺氧最敏感的器官,脑缺氧后会导致局部脑组织受损,当缺血脑组织恢复血流供应后,其损伤反而加重,即脑缺血再灌注损伤。硫化氢(hydrogen sulfide, H2S)是一种气体信号分子,同时也是新型的内源性神经调节物。不同浓度的H2S对神经元的作用有所不同。低浓度的H2S可通过抗氧化应激损伤、抑制炎症反应、抑制细胞凋亡、减轻脑血管内皮细胞损伤、调节细胞自噬等多种途径,在脑缺血再灌注损伤中发挥重要的保护作用,为临床诊治相关疾病提供了新思路。本文就脑缺血再灌注损伤时H2S对损伤脑组织保护作用的最新研究进展作一综述。  相似文献   

5.
Cdk5与大鼠脑缺血再灌注损伤时细胞凋亡的关系   总被引:2,自引:0,他引:2  
目的利用大鼠可逆性大脑中动脉栓塞模型(MCAO),研究周期素依赖性蛋白激酶5(cyclin dependent kinase5,Cdk5)对视网膜母细胞瘤蛋白(Rb)的磷酸化作用与细胞凋亡的关系。方法线栓法制作大鼠MCAO模型,随机分为再灌注0、3、6、9、24h组。通过免疫组化染色观察缺血侧大脑Cdk5和磷酸化Rb的数量和变化,TUNEL标记法检测凋亡神经元数量和变化,Western blot检测不同再灌注时间Cdk5蛋白水平的表达。结果缺血侧cdk5随再灌注时间增加而增加,24h达到高峰;再灌注6h出现磷酸化的视网膜母细胞瘤蛋白(pRb),并随再灌注时间增加而增加,24h达到高峰。缺血侧凋亡阳性细胞变化趋势与Cdk5基本一致。缺血侧Cdk5蛋白的表达随再灌注时间增加而增加,缺血对侧无明显变化。结论大鼠局限性脑缺血再灌注损伤可以诱导Cdk5数量和激酶活性增加,通过底物磷酸化作用引起神经细胞凋亡。  相似文献   

6.
目的:研究orexin-A对缺血再灌注大鼠脑损伤的保护作用。方法:取成年雄性大鼠6只,观察MCAO前和MCAO后2 h、24h的生理学参数,界定后续指标参考时间。另取20只大鼠随机分为MCAO组、vehicle组、orexin-A 50μg/kg组和orexin-A 100μg/kg组(n=5),于缺血再灌注24 h后评估大鼠神经功能学评分和脑梗死容积。再取60只大鼠同样分成4组,(各组n=15),每组在术前、手术后6 h、24 h(各时间点n=5)取脑组织匀浆离心,检测上清液中谷胱甘肽过氧化物酶(GSH-PX)和丙二醛(MDA)的含量。结果:(1)大鼠MCAO术前、术后2 h、24 h生理参数比较无统计学意义(P0.05),提示脑保护参考指标在MCAO后24 h内不受影响。(2)与MCAO组、vehicle组相比,orexin-A 50和100μg/kg降低神经功能评分(P0.05)且梗死容积缩小(P0.05);术前、术后6 h和术后24 h,脑匀浆中GSH-PX活性升高,MDA含量降低(P0.05)。结论:Orexin-A可能通过降低脑内自由基水平,控制脂质过氧化物酶从而对脑缺血再灌注损伤起保护作用。  相似文献   

7.
卢奎  胡斌  黎捷  刘中华  周敏  吴文军 《生物磁学》2013,(35):6806-6809
目的:研究神经调节素及基质金属蛋白酶-9对于小鼠大脑缺血再灌注损伤后炎症反应的抑制作用和机制。方法:选取100只成年雄性大鼠,随机分成对照和治疗组。采用线栓方法由颈内到颈外进行插线处理,造成大脑中动脉处于闭塞状态的再灌注动物模型。治疗组颈动脉进行注射少量NRG-1β干预性治疗,通过氯化三苯基四氮唑(TTC)检查脑梗塞范围,细胞凋亡采用原住脱氧核糖核苷酸末端转移酶介导缺口末端进行标记,采用免疫组织化学、免疫荧光双标记法及免疫印迹法观察脑组织基质金属蛋白酶-9(MMP-9)表达。结果:脑缺血再灌注损伤后,随时间延长及缺氧,对照组大鼠大脑皮质和纹状体区脑组织细胞凋亡,并且胶质细胞MMP-9蛋白表达逐渐增加。治疗组大鼠经注射NRG-1β干预性治疗后,缺血脑组织梗死范围及其细胞凋亡数量相对呈明显下降趋势。胶质细胞MMP-9表达呈降低趋势。结论:大鼠脑缺血再灌注损伤后体内NRG-1β抑制胶质细胞MMP-9的表达,控制缺血脑组织梗死的范围并抑制正常细胞的凋亡,发挥了重要的抗炎作用,可作为对于大脑缺血再灌注损伤的研究新靶点。  相似文献   

8.
目的:探讨十六酰胺乙醇(Palmitoylethanolamide PEA)对大鼠脑缺血再灌注损伤的保护作用及机制。方法:将雄性SD大鼠随机分为:假手术组、药物组、模型组。采用线栓法制造大脑中动脉缺血再灌注模型,药物组于缺血后30分钟及再灌注后2小时给予PEA(10mg/Kg)腹腔注射。于再灌注24h后,对各组大鼠进行神经功能评分,TTC染色法测脑梗死体积,硫代巴比妥法测丙二醛(MDA)含量,黄嘌呤氧化酶法测超氧化物歧化酶(SOD)活性,WesternBlot法测Bcl-2和Bax蛋白含量。结果:药物组神经功能评分均值为1.33±0.49分,而模型组为2.20±0.41分,药物组神经功能评分显著低于模型组(P0.05);药物组的脑梗死体积为114.00±8.63mm3,而模型组脑梗死体积为243.40±14.19mm3,药物组脑梗死体积显著低于模型组(P0.05);药物组MDA含量为3.85±0.29nmol/mgprot,SOD活性为13.95±0.71U/mgprot,而模型组MDA含量为4.85±0.30nmol/mgprot,SOD活性为12.44±0.40U/mgprot,与模型组相比,药物组的MDA含量显著降低,而SOD活性显著增高(P0.05);药物组Bcl-2蛋白与β-action蛋白的IOD值比值为0.53±0.013%,Bax蛋白与β-action蛋白的IOD值比值为0.54±0.012%,模型组Bcl-2蛋白与β-action蛋白的IOD值比值为0.40±0.012%,Bax蛋白与β-action蛋白的IOD值比值为0.80±0.012%。药物组Bax蛋白含量显著低于模型组(P0.05),而Bcl-2蛋白含量显著高于模型组(P0.05)。结论:PEA对大鼠脑缺血再灌注损伤具有保护作用,可能是通过抗凋亡、抗氧化应激等作用实现。  相似文献   

9.
目的:评价钙敏感受体在大鼠脑缺血再灌注损伤时细胞凋亡中的作用。方法:健康成年雄性Wistar大鼠60只,体重250~300 g,采用随机数字表法分为3组(n=20):假手术组(S组)、脑缺血再灌注组(I/R组)和钙敏感受体拮抗剂组(N组)。I/R组和N组采用线栓法经左侧颈外-颈内动脉插线制备大鼠脑缺血再灌注损伤模型,于脑缺血前10 min尾静脉注射等容量二甲基亚砜和钙敏感受体拮抗剂NPS-89636 1 mg/kg。于再灌注24 h时行神经功能评分,随后处死大鼠取脑组织,测定MDA含量和SOD活性,采用TUNEL法观察神经细胞凋亡情况,计算神经细胞凋亡指数,免疫组化法检测Caspase-3阳性细胞的表达,Western blot法检测Caspase-3蛋白的表达。结果:I/R组和N组MDA含量、神经细胞凋亡指数、Caspase-3阳性细胞和Caspase-3蛋白表达水平高于S组,神经功能评分和SOD活性低于S组,差异有统计学意义(P0.05);N组MDA含量、神经细胞凋亡指数、Caspase-3阳性细胞和Caspase-3蛋白表达水平低于I/R组,神经功能评分和SOD活性高于I/R组,差异有统计学意义(P0.05)。结论:钙敏感受体参与大鼠脑缺血再灌注损伤和细胞凋亡的发生。  相似文献   

10.
高压氧对脑缺血再灌注海马CA_1区神经元凋亡作用的研究   总被引:4,自引:0,他引:4  
目的和方法 :应用TUNEL检测技术 ,对沙土鼠前脑缺血 2 0min后再灌注 3d模型 ,用HBO治疗连续 3d。观察HBO作用下海马CA1区神经元凋亡变化 ,研讨HBO对脑缺血再灌注损伤的疗效及其机理 ,为临床应用HBO治疗疾病提供理论依据。结果 :沙土鼠脑缺血再灌注 3d后海马CA1区大量神经元凋亡 ,HBO治疗组凋亡细胞数明显减少 (P <0 .0 1) ,并以 0 .2 5MPaHBO治疗组为佳。结论 :HBO治疗对海马神经元损伤有保护作用 ,减少神经元凋亡 ,为高压氧治疗缺血性损伤的疗效机理之一  相似文献   

11.
12.
Neuregulin-1 (NRG-1), an endogenously produced polypeptide, is the ligand of cardiomyocyte ErbB receptors, with cardiovascular protective effects. In the present study, we explored whether the cardioprotective effect of NRG-1 against I/R injury is mediated by inhibiting myocardial endoplasmic reticulum (ER) stress. In vitro, NRG-1 directly inhibited the upregulation of ER stress markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein and cleaved caspase-12 induced by the ER stress inducers tunicamycin or dithiothreitol in both neonatal and adult ventricular myocytes. Attenuating ErbB signals by an ErbB inhibitor AG1478 or ErbB4 knockdown and preincubation with phosphoinositide 3-kinase inhibitors all reversed the effect of NRG-1 inhibiting ER stress in cultured neonatal rat cardiomyocytes. Concurrently, cardiomyocyte ER stress and apoptosis induced by hypoxia-reoxygenation were decreased by NRG-1 treatment in vitro. Furthermore, in an in vivo rat model of myocardium ischemia/reperfusion (I/R), intravenous NRG-1 administration significantly decreased ER stress and myocardial infarct size induced by I/R. NRG-1 could protect the heart against I/R injury by inhibiting myocardial ER stress, which might be mediated by the phosphoinositide 3-kinase/Akt signaling pathway.  相似文献   

13.
目的:探讨电针促进局灶脑缺血/再灌注后缺血海马区血管再生的机制。方法180只雄性SD大鼠随机分为假手术组、模型组、电针组、CXCR4特异性拮抗剂AMD3100药物组、AMD3100+电针组。线栓法制备右侧局灶脑缺血/再灌注模型。取大鼠“百会”穴( GV 20)及左侧“四关”穴(合谷LI 4/太冲LR 3)为电针穴位,刺激时间为30 min/d。采用逆转录聚合酶链反应法( RT-PCR)检测各组缺血海马区SDF-1α、CXCR4 mRNA表达,免疫荧光双标法检测CD34+VEGFR2+EPCs源性血管的表达。结果与假手术组比较,模型组与电针组SDF-1α、CX-CR4 mRNA表达明显增高(P<0.05),其中电针组各时间点相对模型组增高更为显著(P<0.05)。 AMD3100+电针组缺血海马SDF-1α、CXCR4 mRNA表达在再灌注后1 d时明显高于电针组( P<0.05),但后逐渐下降,7 d时明显低于电针组( P<0.01)。与模型组比较,电针组再灌注3 d、7 d海马CD34+VEGFR2+EPCs源性血管表达明显增多( P<0.05)。与电针组比较,AMD3100+电针组再灌注后7 d CD34+VEGFR2+EPCs源性血管表达明显下降( P<0.01)。 CD34+VEGFR2+血管表达变化与SDF-1α的表达变化显著相关(R=0.784,P<0.01)。结论电针可通过上调局灶脑缺血/再灌注大鼠缺血海马区SDF-1α/CXCR4的表达,促进血管再生。  相似文献   

14.
目的: 探讨早期跑步运动对大鼠脑缺血后神经行为与神经元凋亡的影响。方法:雄性SD大鼠随机分为4组:假手术+安静组(Sham-St、假手术+运动组(Sham-Ex)、缺血(大脑中动脉闭塞(MCAO) +运动组((MCAO -Ex)和缺血+安静组(MCAO-St),每组15只。MCAO-Ex 和 MCAO-St 组大鼠行MCAO 60 min,再灌注2 d后,MCAO-Ex 和Sham-Ex大鼠在跑步机上进行5 d的30 min/d跑步运动(15 m/min),之后进行神经行为学评价,最后大鼠断头取脑进行TTC方法染色,评估各组大鼠梗死体积以及缺血半影Caspase-3和TUNEL阳性细胞表达水平。结果:与Sham-St相比,MCAO-St和MCAO-Ex大鼠缺血半影区Caspase-3表达均显著升高 (P<0.05);与MCAO-St 组大鼠相比,MCAO-Ex组大鼠脑梗死体积明显减少,大鼠神经功能评分明显改善,大鼠缺血半影区Caspase-3和TUNEL阳性细胞表达水平显著降低 (P<0.05)。结论: 早期运动可能通过抑制大鼠脑缺血后神经元凋亡发挥神经保护作用。  相似文献   

15.
目的:探讨缺血后处理对再灌注损伤肺细胞凋亡的影响。方法:健康雄性sD大鼠24只,随机分为对照组(C组)、缺血/再灌注组(I/n组)和缺血后处理组(IPostC组)(n=8)。对比观察各组血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活力及含量变化,原位缺口末端标记法(TUNEL)检测肺组织细胞凋亡情况,免疫组化及RT-PCR法检测肺组织中Bax、Bcl一2蛋白和基因的表达。结果:I/R组与c组相比,MDA含量、MPO活力明显升高,SOD活力明显下降(均P〈0.01),肺组织原位细胞凋亡检测示I/R组凋亡指数(AI)(39.03±3.46)显著高于C组(2.88±0.34),Bcl-2/Bax比值在蛋白和基因水平明显降低(均P〈0.01);IPostC组与I/R组相比MDA含量显著降低(P〈0.05),MPO活力显著降低(P〈0.01),SOD活性升高(P〈0.01),AI为8.03±0.88显著低于L/R组,并能明显升高Bcl-2/Bax比值(均P〈0.01)。结论:缺血后处理通过减轻脂质过氧化反应及中性粒细胞聚集,降低Bax/Bel.2比值,使肺组织细胞凋亡减少,从而有效地减轻肺缺血/再灌注损伤。  相似文献   

16.
The receptor tyrosine kinases ErbB2 and ErbB3 are phosphorylated in response to injury of the airway epithelium. Since we have shown that the membrane mucin MUC4 can act as a ligand/modulator for ErbB2, affecting its localization in polarized epithelial cells and its phosphorylation, we questioned whether Muc4 was involved, along with ErbB2 and ErbB3, in the damage response of airway epithelia. To test this hypothesis, we first examined the localization of MUC4 in human airway samples. Both immunocytochemistry and immunofluorescence showed a co‐localization of MUC4 and ErbB2 at the airway luminal surface. Sequential immunoprecipitation and immunoblotting from airway cells demonstrated that the MUC4 and ErbB2 are present as a complex in airway epithelial cells. To assess the participation of MUC4 in the damage response, cultures of NCI‐H292 or airway cells were scratch‐wounded, then analyzed for association of phospho‐ErbB2 and ‐ErbB3 with MUC4 by sequential immunoprecipitation and immunoblotting. Wounded cultures exhibited increased phosphorylation of both receptors in complex with MUC4. Scratch wounding also increased activation of the downstream pathway through Akt, as predicted from our previous studies on Muc4 effects on ErbB2 and ErbB3. The participation of MUC4 in the phosphorylation response was also indicated by siRNA repression of MUC4 expression, which resulted in diminution of the phosphorylation of ErbB2 and ErbB3. These studies provide a new model for the airway epithelial damage response, in which the MUC4–ErbB2 complex is a key element in the sensor mechanism and phosphorylation of the receptors. J. Cell. Biochem. 107: 112–122, 2009. © 2009 Wiley‐Liss, Inc.  相似文献   

17.
一种用于研究骨骼肌缺血/再灌注损伤的细胞模型   总被引:3,自引:1,他引:3  
目的:复制L-6TG大鼠肌母细胞缺血/再灌注损伤的细胞模型.方法:将培养的L-6TG大鼠肌母细胞随机分为2组:①正常对照组(C组),②缺血/再灌注组(I/R组),观测了培养上清中乳酸脱氢酶(LDH)、细胞内超氧化物歧化酶(SOD)、黄嘌呤氧化酶(XOD)、Ca2 含量的变化;采用MTT法检测线粒体的功能;在光镜下观察细胞的形态学改变.结果:与对照组相比,L-6TG大鼠肌母细胞IR 4h后培养上清中LDH、细胞内XOD、Ca2 含量明显增加,细胞内SOD及线粒体呼吸功能明显降低,细胞严重受损,明显圆缩,并有脱落现象.结论:应用模拟缺血液和再灌液可成功复制L-6TG大鼠肌母细胞缺血/再灌注损伤的细胞模型.  相似文献   

18.
Currently, the prevention of ischemic diseases such as myocardial infarction associated with ischemia/reperfusion (I/R) injury remains to be a challenge. Thus, this study was designed to explore the effects of tripartite motif protein 11 (TRIM11) on cardiomyocytes I/R injury and its underlying mechanism. Cardiomyocytes AC16 were used to establish an I/R injury cell model. After TRIM11 downregulation in I/R cells, cell proliferation (0, 12, 24, and 48 h) and apoptosis at 48 h as well as the related molecular changes in oxidative stress-related pathways was detected. Further, after the treatment of TRIM11 overexpression, SP600125, or DUSP1 overexpression, cell proliferation, apoptosis, and related genes were detected again. As per our findings, it was determined that TRIM11 was highly expressed in the cardiomyocytes AC16 after I/R injury. Downregulation of TRIM11 was determined to have significantly reduced I/R-induced proliferation suppression and apoptosis. Besides, I/R-activated c-Jun N-terminal kinase (JNK) signaling and cleaved caspase 3 and Bax expression were significantly inhibited by TRIM11 downregulation. In addition, the overexpression of TRIM11 significantly promoted apoptosis in AC16 cells, and JNK1/2 inhibition and DUSP1 overexpression potently counteracted the induction of TRIM11 overexpression in AC16 cells. These suggested that the downregulation of TRIM11 attenuates apoptosis in AC16 cells after I/R injury probably through the DUSP1-JNK1/2 pathways.  相似文献   

19.
牛磺酸对家兔缺血/再灌注心肌细胞凋亡的影响   总被引:2,自引:0,他引:2  
Li AY  Ji ES  Zhao SM  Ma ZH  Li Q 《中国应用生理学杂志》2004,20(3):224-227,F005
目的:研究牛磺酸(Tau)对家兔缺血/再灌注损伤心肌细胞凋亡的影响.方法:阻断家兔心脏左冠状动脉前降支45 min,再灌注180 min引起心肌缺血/再灌注损伤,在心肌缺血前5 min耳缘静脉注射牛磺酸(200mg/kg),应用DNA片段原位末端标记法 (TUNEL染色),DNA凝胶电泳和流式细胞仪(FCM)观测心肌细胞凋亡.结果:琼脂糖凝胶电泳显示损伤对照组(I/R) 心肌DNA呈云梯状改变,而Tau I/R组无此改变.与损伤对照组(I/R) 比较,Tau I/R组缺血心肌凋亡细胞明显减少(TUNEL染色).流式细胞仪测定I/R组及Tau I/R组缺血心肌凋亡率分别为17.66%±1.54%和4.86%±1.23%.I/R组的缺血心肌Fas和Bax蛋白表达较非缺血心肌高 (P<0.01),Bcl-2/Bax比例较非缺血心肌低(P<0.01);而在Tau I/R组,Fas和Bax蛋白表达较I/R组的低 (P<0.01),Bcl-2/Bax比例较I/R组高(P<0.01).结论:牛磺酸可减少I/R家兔心肌细胞凋亡,其机制与调控凋亡相关基因 Fas,Bax和Bcl-2的蛋白表达有关.  相似文献   

20.

Objective

Explore the possible protective effect of Sargentodoxa cuneata total phenolic acids on cerebral ischemia reperfusion injury rats.

Methods

Focal cerebral ischemia reperfusion rats model were established by linear thrombus. Nimodipine group, Naoluotong group, the high, middle and low dose of Sargentodoxa cuneata total phenolic acids groups were given related drugs via intragastric administration before operation for seven days, once a day. At the same time sham operation group, and ischemia reperfusion group were given the same volume of physiological saline. One hour after the last administration, establish focal cerebral ischemia- reperfusion model in rats by thread method, and the thread was taken out after 2?h ischemia to achieve cerebral ischemia reperfusion injury in rats. After reperfusion for 24?h, the rats were given neurologic deficit score. The brain tissue was taken to measure the levels of IL-6, IL-1β, TNF-α, Bcl-2, Bax, Casp-3 and ICAM-1; HE staining observed histopathological changes in the hippocampus and cortical areas of the brain; Immunohistochemistry was used to observe the expression of NGF and NF-KBp65.

Result

Focal cerebral ischemia reperfusion rats model was copyed successed. Compared with model group, each dose group of Sargentodoxa cuneata total phenolic acids could decreased the neurologic deficit score (P?<?0.05 or P?<?0.01), decreased the levels of IL-6, IL-1β, ICAM-1, TNF-α, Bax and Caspase-3 in brain tissue (P?<?0.05 or P?<?0.01), increased the levels of IL-10, Bcl-2, NGF in brain tissue (P?<?0.05 or P?<?0.01), decreased the express of NF-KBp65 in brain (P?<?0.05 or P?<?0.01).

Conclusion

Sargentodoxa cuneata total phenolic acids can improve focal cerebral ischemia reperfusion injury rats tissue inflammation, apoptosis pathway, increase nutrition factor to protect the neurons, reduce the apoptosis of nerve cells, activate brain cells self-protect, improve the histopathological changes in the hippocampus and cortical areas of the brain, reduce cerebral ischemia reperfusion injury.  相似文献   

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