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1.
Rho激酶,又称Rho相关的卷曲蛋白激酶,是一类丝氨酸/苏氨酸蛋白激酶,被发现为小G蛋白Rho的下游作用底物。由于Rho激酶活性涉及神经细胞的功能,而且越来越多的研究表明抑制Rho激酶的活性在数种神经退行性疾病包括帕金森病、阿尔茨海默病、亨廷顿病、多发性硬化症,和肌萎缩性侧索硬化症等的实验模式中都有明显的效果。因此,Rho激酶已成为针对治疗神经性退化性疾病的一个热门标靶蛋白。本文探讨Rho激酶抑制剂在神经退化性疾病上的应用及发展,使神经退行性疾病能进一步提升治疗和在应用上的水平。  相似文献   

2.
已知Rho激酶抑制剂可调控细胞骨架重建,激活相关转录因子,进而促进细胞分化。然而,关于Rho激酶抑制剂对细胞骨架和成骨细胞分化的影响及两者之间关系尚未见报道。本研究旨在阐明Rho激酶抑制剂Y-27632调控细胞骨架重建,促进成骨分化。取新生SD大鼠头盖骨组织体外培养细胞传至第3代,给予Rho激酶抑制剂Y-27632进行干预。采用罗丹明标记的鬼笔环肽对细胞骨架进行细胞化学染色。结果显示,培养1 d和2 d,Rho激酶抑制剂Y-27632处理的细胞呈现多角形,并伴有部分伪足形成。细胞培养4 d和7 d,Y-27632处理的细胞碱性磷酸酶(alkaline phosphatase,ALP)活性明显增加(P0.01)。实时定量PCR揭示,加Y-27632处理细胞的骨分化相关基因Runx2、Alp、β-catenin(β-cat)、osteopontin(Opn)的mRNA表达水平均显著高于对照细胞(P0.05或P0.01)。以上结果证明,Rho激酶抑制剂Y-27632能够影响大鼠成骨细胞的形态,并有促进其分化作用。本研究为骨代谢疾病及组织工程的研究提供了新的线索和启示。  相似文献   

3.
目的:分析急性心肌梗死(AMI)后大鼠心肌组织Rho激酶表达的变化及心肌细胞凋亡情况,观察法舒地尔对急性心肌梗死(AMI)后大鼠心肌组织Rho激酶表达的影响,探讨法舒地尔对心梗后心肌的保护作用。方法:选取雄性Wistar大鼠,随机分为三组:治疗组、AMI组、假手术组。治疗组及AMI组均结扎左前降支(LAD)制作AMI模型;假手术组只在其LAD下穿线不结扎。治疗组给予法舒地尔5mg/kg,腹腔注射,每日两次;对照组和假手术组给予等量生理盐水。1周后,EvensBlue及NBT双染色确定缺血面积及梗死面积,RT-PCR法测定rho激酶mRNA的表达,DNA断裂的原位末端标记法(T UNEL法)检测缺血区心肌细胞凋亡指数(AI),免疫组化测定凋亡相关蛋白bcl-2及bax表达的变化。结果:1周后,AMI组与假手术组相比,AMI组大鼠Rho激酶mRNA表达增加(P0.01),凋亡相关蛋白bax表达增加(P0.01),bcl-2表达减少(P0.01),AI明显增加(P0.01)。治疗组与AMI组相比,梗死面积显著减小(P0.05),Rho激酶mRNA及bax表达显著减少,AI显著降低,bcl-2表达显著增加(均P0.01)。结论:大鼠AMI后,心肌组织中Rho激酶的表达增加,心肌细胞凋亡指数增加,连续应用法舒地尔1周能有效减少心肌细胞凋亡指数,起到心肌保护的作用。  相似文献   

4.
目的探讨Rho A/ROCK信号通路在左心疾病相关的大鼠肺动脉高压模型中的表达水平和作用。方法 3~4周龄雄性SD大鼠20只,体重90~100 g,随机分为对照组(C组:n=10)、肺高压组(H组:n=10)。H组采用升主动脉固定缩窄术建造左心疾病相关肺动脉高压大鼠模型,C组大鼠行假手术处理(钛夹固定于血管旁纵隔组织而非升主动脉,其他所有手术操作同H组),在建模后60 d,对各组大鼠进行血流动力学(右心室收缩压、肺动脉压力)检测,处死大鼠并用PBS行在体心肺灌洗致双肺变白,左肺组织固定于4%多聚甲醛行病理切片以观察肺组织病理形态学变化、右肺组织冻存以备生物分子学检测(Rho激酶mRNA、Rho A mRNA、ET-A受体mRNA)。结果与C组相比,H组肺动脉压力、右心室收缩压明显增高(P0.01),肺小动脉壁明显增厚,肺小动脉管腔狭窄甚至闭塞,管壁肥厚指数明显增大(P0.01);与C组相比,H组肺组织的Rho激酶mRNA表达水平明显增加,Rho A mRNA、ET-A受体mRNA表达水平亦明显增加,差异均有统计学意义(P0.01)。结论采用升主动脉固定缩窄术成功建造了左心疾病相关肺动脉高压大鼠模型;与C组相比,H组肺小血管壁明显增厚,肺组织的Rho激酶mRNA、Rho A mRNA、ET-A受体mRNA表达明显增高,该信号通路可能参与了左心疾病相关肺动脉高压的形成过程。  相似文献   

5.
目的应用自制降温线圈发展一种硬膜外局部低温治疗方法,对其降温效能和安全性进行评估。方法SD大鼠随机分为常温对照组(Nor组)、硬膜外局部低温组(LH组)和全身低温组(SH组),对LH组和SH组分别实施硬膜外局部降温和全身降温,观察降温前后同侧脑温、对侧脑温、肛温以及呼吸、心率、血压变化,降温后24h对各组大鼠进行神经功能评测,取脑组织标本行光镜、电镜检查,并检测脑组织水、钠、钾离子含量和血脑屏障通透性。结果降温后,LH组大鼠的降温侧脑温在数分钟内从(36.5±0.3)℃下降到(31.4±0.4)℃并维持稳定,其对侧脑温和肛温无明显下降,R、HR和MABP无明显变化;SH组降温后双侧脑温、肛温均出现降低,降温后HR下降。降温后,LH组和SH组大鼠神经功能评分正常,光镜和电镜下脑组织无损伤表现,其脑组织水、钠、钾离子含量和血脑屏障通透性与常温对照组比较无统计学差异。结论应用这种硬膜外局部低温方法可以达到与全身降温一样的效果,且不会引起生命体征波动及对脑组织产生急性损害。  相似文献   

6.
实验用Wistar大鼠62只,采用束缚加悬吊的方法引起应激性高血粘度和血压升高。结果观察到,清醒大鼠束缚加悬吊二天可引起应激性高血粘度和血压升高。第四脑室内注射5-羟色胺(5-HT25μg/10μl)或在双侧延髓腹外侧区头端(rVLM)微量注射5-HT(4μg/0.5μl/每侧)均可抑制应激性高血粘度和血压升高,若预先在双侧rVLM微量注射5-HT受体阻断剂肉桂硫胺(4μg/0.5μl/每侧)后再在第四脑室或延髓腹外侧区内注入上述同剂量的5-MT,则5-HT降低应激性高血粘度和血压升高的作用消失。看来上述5-HT的作用是通过rVLM内5-HT受体的激活来实现的。  相似文献   

7.
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   

8.
目的对血管性痴呆(VD)大鼠模型的造模方法进行改进,使血管性痴呆的实验研究更加科学可靠。方法采用"反复夹闭颈动脉加注射硝普钠降压再加单侧永久结扎颈总动脉法"制备VD大鼠模型,并用脑复康(吡拉西坦)加以模型验证。实验从大鼠行为学和组织病理两个方面评价VD模型。结果实验结果显示:对比假手术组,模型组大鼠定位航行潜伏期延长,空间搜索穿越平台次数减少,海马病理切片显示:细胞数量较少、细胞轮廓模糊皱缩、胞质深染、核不清晰;脑复康阳性药物对照组上述指标明显改善。结论硝普钠注射量为2.0 mg/kg时,手术室温控制在28℃且术后24 h内控制在25℃,大鼠状态稳定,死亡数减少;术中反复阻断三次双侧颈总动脉后直接永久性结扎左侧颈总动脉,可以切断大约三分之一的脑供血,造成慢性脑供血不足状态,更接近VD发病机制。  相似文献   

9.
血管外膜成纤维细胞表型转化为肌成纤维细胞是血管重塑的重要病理特征。本研究旨在探讨小分子G蛋白RhoA及其下游Rho激酶信号通路在转化生长因子β1(transforming growth factor β1,TGF-β1)诱导的血管外膜成纤维细胞/肌成纤维细胞表型转化中的作用。用10ng/mLTGF-β1诱导体外培养的大鼠胸主动脉外膜成纤维细胞表型转化为肌成纤维细胞,使用亲和沉淀法检测RhoA活性、使用免疫印迹检测RhoA、Rho激酶蛋白表达和Rho激酶活性;使用免疫印迹和免疫细胞化学检测肌成纤维细胞标记蛋白的表达。结果显示,TGF-β1上调体外培养的血管外膜成纤维细胞RhoA蛋白表达和RhoA活性。TGF-β1增加Rho激酶下游底物肌球蛋白磷酸酶目标亚单位的磷酸化,但不改变Rho激酶的蛋白表达,提示TGF-β1增加Rho激酶活性。腺病毒Ad-N19RhoA-hrGFP感染和Rho激酶特异性抑制剂Y27632都呈剂量依赖性地抑制TGF-β1诱导的肌成纤维细胞标记分子α平滑肌肌动蛋白和钙结合蛋白Calponin的蛋白表达。本研究证明RhoA-Rho激酶信号通路参与了TGF-β1诱导的血管外膜成纤维细胞/肌成纤维细胞表型转化。  相似文献   

10.
目的:观察中枢nesfatin-1对大鼠夜间摄食和胃排空的影响。方法:大鼠经腹腔注射硫酸仲丁巴比妥(100~150 mg/kg)麻醉,侧脑室、第四脑室或小脑延髓池注射nesfatin-1或CRF受体拮抗剂astressin-B或astressin2-B,观察对摄食、胃排空的影响。结果:侧脑室注射nesfatin-1后大鼠第3-6 h夜间进食量(t=3.05~3.58,P0.01)和3 h和6 h的累积进食量(t=5.90~12.1,P0.01)明显减少,nesfatin-1的该抑制效应可被预先侧脑室注射astressin-B或astressin2-B阻断(t=1.06~2.22,P0.05)。第四脑室或小脑延髓池注射nesfatin-1后大鼠夜间摄食量在第1h就明显减少(t=2.59~6.26,P0.05~0.01),持续减少至5-6h(t=1.69~7.42,P0.05~0.01)。侧脑室注射不同剂量nesfatin-1(0.05或0.5μg)20 min后GE率明显降低,且随注射剂量增大,GE率越低(t=3.25~4.67,P0.01)。若预先给予大鼠CRF受体拮抗剂astressin2-B(30μg)再注射nesfatin-1(0.5μg),nesfatin-1抑制大鼠胃排空效应明显减弱(t=2.45~2.85,P0.05)。禁食24 h后再喂食2 h,大鼠下丘脑中nesfatin-1表达明显增加(t=2.87,P0.05),禁食24 h后血浆nesfatin-1水平明显降低(t=1.51,P0.05)。结论:Nesfatin-1抑制摄食作用可能由nesfatin-1和CRF2信号系统共同调节。  相似文献   

11.
The objective of the present study was to examine the role of the angiotensin II type 1 receptor (AT(1)-R) in the diabetes-aggravated oxidative stress and brain injury observed in a rat model of combined diabetes and focal cerebral ischemia. Diabetes was induced by an injection of streptozotoxin (STZ; 55 mg/kg iv) at 8 wk of age. Two weeks after the induction of diabetes, some animals received continuous subcutaneous infusion of the AT(1)-R antagonist candesartan (0.5 mg.kg(-1).day(-1)) for 14 days. Focal cerebral ischemia, induced by middle cerebral artery occlusion/reperfusion (MCAO), was conducted at 4 wk after STZ injection. Male Sprague-Dawley rats (n = 189) were divided into five groups: normal control, diabetes, MCAO, diabetes + MCAO, and diabetes + MCAO + candesartan. The major observations were that 1) MCAO produced typical cerebral infarction and neurological deficits at 24 h that were accompanied by elevation of NAD(P)H oxidase gp91(phox) and p22(phox) mRNAs, and lipid hydroperoxide production in the ipsilateral hemisphere; 2) diabetes enhanced NAD(P)H oxidase gp91(phox) and p22(phox) mRNA expression, potentiated lipid peroxidation, aggravated neurological deficits, and enlarged cerebral infarction; and 3) candesartan reduced the expression of gp91(phox) and p22(phox), decreased lipid peroxidation, lessened cerebral infarction, and improved the neurological outcome. We conclude that diabetes exaggerates the oxidative stress, NAD(P)H oxidase induction, and brain injury induced by focal cerebral ischemia. The diabetes-aggravated brain injury involves AT(1)-Rs. We have shown for the first time that candesartan reduces brain injury in a combined model of diabetes and cerebral ischemia.  相似文献   

12.
The blood-brain barrier (BBB) disruption and brain edema are important pathophysiologies of early brain injury after subarachnoid hemorrhage (SAH). This study is to evaluate whether Rho kinase (Rock) enhances BBB permeability via disruption of tight junction proteins during early brain injury. Adult male rats were assigned to five groups; Sham-operated, SAH treated with saline, a Rock inhibitor hydroxyfasudil (HF) (10 mg/kg) treatment at 0.5 h after SAH, HF treatment at 0.5 and 6 h (10 mg/kg, each) after SAH, and another Rock inhibitor Y27632 (10 mg/kg) treatment at 0.5 h after SAH. The perforation model of SAH was performed and neurological score and brain water content were evaluated 24 and 72 h after surgery. Evans blue extravasation, Rock activity assay, and western blotting analyses were evaluated 24 h after surgery. Treatment of HF significantly improved neurological scores 24 h after SAH. Single treatment with HF and Y27632, and two treatments with HF reduced brain water content in the ipsilateral hemisphere. HF reduced Evans blue extravasation in the ipsilateral hemisphere after SAH. Rock activity increased 24 h after SAH, and HF reversed the activity. SAH significantly decreased the levels of tight junction proteins, occludin and zonula occludens-1 (ZO-1), and HF preserved the levels of occluding and ZO-1 in ipsilateral hemisphere. In conclusion, HF attenuated BBB permeability after SAH, possibly by protection of tight junction proteins.  相似文献   

13.
In a model of cerebral hypoxia-ischemia in the immature rat, widespread brain injury is produced in the ipsilateral hemisphere, whereas the contralateral hemisphere is left undamaged. Previously, we found that calpains were equally translocated to cellular membranes (a prerequisite for protease activation) in the ipsilateral and contralateral hemispheres. However, activation, as judged by degradation of fodrin, occurred only in the ipsilateral hemisphere. In this study we demonstrate that calpastatin, the specific, endogenous inhibitor protein to calpain, is up-regulated in response to hypoxia and may be responsible for the halted calpain activation in the contralateral hemisphere. Concomitantly, extensive degradation of calpastatin occurred in the ipsilateral hemisphere, as demonstrated by the appearance of a membrane-bound 50-kDa calpastatin breakdown product. The calpastatin breakdown product accumulated in the synaptosomal fraction, displaying a peak 24 h post-insult, but was not detectable in the cytosolic fraction. The degradation of calpastatin was blocked by administration of CX295, a calpain inhibitor, indicating that calpastatin acts as a suicide substrate to calpain during hypoxia-ischemia. In summary, calpastatin was up-regulated in areas that remain undamaged and degraded in areas where excessive activation of calpains and infarction occurs.  相似文献   

14.
Hwang YS  Shin CY  Huh Y  Ryu JH 《Life sciences》2002,71(18):2105-2117
The preventive effect of Hwangryun-Hae-Dok-tang (HHDT, Huanglian-Jie-Du-Tang), a Chinese herbal medicine, and its ingredients on ischemia/reperfusion-induced brain injury was evaluated in the rat brain. HHDT consists of four herbs, namely, Coptidis rhizoma, Scutellariae radix, Phellodendri cortex, and Gardeniae fructus. Ischemia was induced by intraluminal occlusion of the right middle cerebral artery for 120 min and reperfusion was continued for 22 h. HHDT (200 mg/kg), Coptidis rhizoma (100 mg/kg), Scutellariae radix (100 mg/kg), Phellodendri cortex (100 mg/kg), and Gardeniae fructus (100 mg/kg) were orally administered, promptly prior to reperfusion and 2 h after reperfusion. Baicalein, a component of Scutellariae radix, was also examined at a dosage of 50 mg/kg given 2 h apart, promptly prior to and 2 h after reperfusion. Total infarction volume in the ipsilateral hemisphere of ischemia/reperfusion rats was significantly lowered by treatment with HHDT, Scutellariae radix, and balicalein. However, the other ingredient of HHDT did not show any ameliorating effects on total infarction volume. The inhibiting effect of Scutellariae radix on total infarction volume was much higher than that of the others. In addition, HHDT, Scutellariae radix, and baicalein significantly inhibited myeloperoxidase (MPO) activity, an index of neutrophil infiltration in ischemic brain tissue at about the same rate (30%). There was marked mismatch between total infarction volume and MPO activity in the Scutellariae radix-treated rats but not in the HHDT- and baicalein-treated groups. Our findings suggest that Scutellariae radix as an ingredient of HHDT plays a crucial protective role in ischemia-induced brain injury. In addition, it is apparent that the effect of Scutellariae radix is the result, in part, of baicalein, a compound contained in Scutellariae radix.  相似文献   

15.
C6 cells were used to establish a glioma-bearing rat model by stereotaxic injection in the left caudate nucleus. The tumor status was evaluated by magnetic resonance imaging and conventional histology. The glioma-bearing rats were infused for 1 h with a [1-(13)C]glucose solution. Perchloric acid extracts of the tumor and the ipsilateral and contralateral hemispheres were analyzed by 13C-NMR spectroscopy. The 13C-labeling patterns in compounds, mainly amino acids, indicated no drastic modification of carbon metabolism in both ipsilateral and contralateral hemispheres, as compared with control rats, whereas profound metabolic differences between brain tissue and tumor were observed. Glutamine C4 enrichment was lower in the glioma than in the brain [mean +/- SD values, 5.4 +/- 2.3 (n = 5) and 15.0 +/- 0.8% (n = 10), respectively] and also lower than the glutamate C4 enrichment in the glioma (mean +/- SD value, 22.6 +/- 4.2%; n = 5), indicating that tumor glutamine was neither synthesized inside the glioma nor taken up from the surrounding brain. The glutamine C4 enrichment in the serum (6.7 +/- 0.5%; n = 10) suggested that the glioma imported glutamine from the blood, a process probably connected with angiogenesis.  相似文献   

16.
Various reports in the literature have shown that hyperbaric oxygen (HBO) reduces cerebral infarction both in animals and humans. After the initial ischemic insult, however, initiating HBO treatment at different intervals has yielded conflicting results. The present study was undertaken to determine the optimal therapeutic window in which to start HBO treatment for cerebral infarction after transient focal ischemia. In this study, the operator occluded the middle cerebral artery (MCA) of anesthetized rats by introducing a blunted nylon filament into the proximal MCA from the dissected external carotid artery. When the operator removed the filament after 2 h, focal ischemia and reperfusion occurred. The operator then placed the rat in the HBO chamber and administered 3 atm absolute HBO for 1 h according to the protocol. The rat was killed 24 h after reperfusion, and the percentage of infarction (infarct ratio) was calculated by dividing the infarction area by the total area of the ipsilateral hemisphere. The results showed that the percentage of infarcted area decreased significantly (P < 0.05) both in the 3- (7.59%) and 6-h (5.35%) HBO-treatment groups compared with the control (no treatment) group (11.34%). However, the percentage of infarcted area increased significantly (P < 0.01 and P < 0.05, respectively) both in the 12- (23%) and 23-h (20%) treatment groups. The results of this study suggest that applying HBO within 6 h of ischemia-reperfusion injury could benefit the patient but that applying HBO 12 h or more after injury could harm the patient.  相似文献   

17.
18.
The major cholinergic innervation of the rat cerebral cortex arises from the nucleus basalis in the basal forebrain. Introduction of the excitotoxins kainate or ibotenate into the nucleus basalis by stereotaxic injection results in degeneration of the cholinergic cells. We have investigated the effect of this excitotoxic action on ornithine decarboxylase (ODC) activity and cholinergic responsiveness in the cerebral cortex. A massive and rapid induction of ODC activity was seen in ipsilateral cortex after injection of excitotoxin. A maximal increase in ODC activity of 268 times the control value was seen in ipsilateral cerebral cortex 8 h after lesioning. Thereafter, ODC activity declined but remained significantly greater than control levels for 32 h. Pretreatment of animals with the irreversible ODC inhibitor difluoromethylornithine prevented the induction of ODC by kainate. Tissue content of the ODC product putrescine showed a marked increase in cerebral cortex ipsilateral to the lesion, increasing sevenfold at 24 h, the maximal concentration reached. After 24 h, the level of putrescine decreased but remained significantly elevated above control values for 5 days. Levels of the polyamines spermidine and spermine were unaffected by lesioning. Increases on ODC activity of much smaller magnitude were also seen in brain regions not directly innervated from the ipsilateral nucleus basalis. However, the response in ipsilateral cortex was found to be dependent on an intact projection from nucleus basalis to cortex. The induction of ODC was shown to be prevented by treatment of rats with MK-801, a result indicating the involvement of N-methyl-D-aspartate (NMDA) receptors.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

19.
原花青素对脑缺血再灌损伤大鼠模型的影响   总被引:1,自引:0,他引:1  
目的研究原花青素对脑缺血/再灌损伤(ischemia/reperfusion,I/R)大鼠神经功能评分(neurologicaldeficit score,NDS)、脑梗死体积、脑含水量等指标的药理作用。方法采用大鼠大脑中动脉阻断(middle cerebralartery occlusion,MCAO)法复制类似人类缺血性卒中的I/R损伤模型。结果该模型各时间点内均有程度不同的神经功能缺失,原花青素给药组神经功能评分明显低于对照组(P0.05),假手术组大鼠均无神经功能缺失,脑水肿情况均较对照组明显改善(P0.05),脑梗死体积与盐水对照组相比差异有显著性(P0.05),而假手术组均未见有梗死灶。结论原花青素具有一定的保护大鼠I/R后受损脑组织的作用,可供后续研究,并可为缺血性卒中使用原花青素治疗提供确凿的理论依据。  相似文献   

20.
To investigate the protective mechanism of verbenalin on cerebral ischemia-reperfusion injury. Middle cerebral artery occlusion in the left hemisphere was induced in rats by filament insertion, and rat model of focal cerebral ischemia-reperfusion was established. The high, medium and low dose of verbenalin groups were injected in the tail vein of corresponding drugs 10?min before reperfusion, and submitted for 22?h of reperfusion after the operation. Mortality rate was then calculated, and neurological deficits of rats were scored. The serum of rats was got to determine the S-100β protein level, and the brain tissue was removed to determine the levels of Bax, Bcl-2, Caspase-3 and ATPase. TTC staining was performed on the brain tissue to calculate the percentage of cerebral infarct size. Changes in brain tissue morphology were observed. Rat model of focal cerebral ischemia-reperfusion was successfully replicated. In groups that have taken different doses of verbenalin, the mortality rate, neurological deficit score and the percentage of cerebral infarction size were significantly reduced, and the levels of Bax, Caspase-3, S-100β level of the serum in the brain tissue were also significantly reduced. Increases in the levels of Bcl-2 and ATPase in brain tissue and improvement of pathological damage of hippocampus and cortex were observed. Verbenalin can inhibit the expression of apoptosis genes, promote the expression of anti-apoptosis genes, improve brain microcirculation and energy metabolism, hence reducing cerebral ischemia-reperfusion injury.  相似文献   

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