共查询到20条相似文献，搜索用时 15 毫秒
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
目的：观察抑郁大鼠模型急性期额叶及海马区Rho激酶（ROCK）的表达变化,探讨Rho／ROCK通路是否与抑郁症形成有关。方法：建立Wistar大鼠抑郁症模型;在建模成功后24h迅速断头取前脑,在冰浴上分离出双侧前额叶及海马脑组织,应用Westernblot分别测定大鼠额叶及海马脑组织内ROCKⅠ及ROCKⅡ含量。结果：与正常对照组比,抑郁模型大鼠左侧和右侧前额叶ROCKⅠ表达均显著增高（分别P〈0．01,P〈0．05）,以左侧为著;ROCKⅡ表达亦有显著增高（均P〈0．05）。抑郁模型大鼠左右侧海马区域ROCKI表达显著增高（分NP〈0．05,P〈0．01）,以右侧明显;ROCKⅡ表达亦有显著增高（分别P〈0．05,P〈0．01）。结论：ROCKⅠ及ROCKⅡ可能参与了抑郁症形成的病理过程。 相似文献
12.
Rho是GTP酶Rho家族中调节肌动蛋白细胞骨架最具特征的成员之一,其最经典的下游底物是Rho激酶(ROCK)。最新研究表明,Rho/ROCK信号通路除了参与缺血性卒中血流动力学障碍及炎症反应以外,还可直接作用于神经元,从而直接导致生长锥塌陷及神经突起回缩。Rho/ROCK信号通路的抑制能够促进中枢神经系统受损后轴突的再生和功能的恢复。目前,ROCK抑制剂之一盐酸法舒地尔(Fasudil)已应用于临床,尤其是在脑血管疾病的治疗中具有广阔的应用前景。 相似文献
13.
Rho/ROCK是机体各组织中普遍存在的一条信号转导通路,介导的信号通路参与细胞的收缩、黏附、迁移、增殖、细胞骨架的形成等多种细胞生物学行为和功能[1-2]。目前越来越多的证据表明,Rho/ROCK在神经系统疾病的发生发展中具有重要作用,对Rho/ROCK信号通路的研究将为某些神经系统疾病的诊断治疗提供新的思路。 相似文献
14.
Rho相关蛋白激酶(ROCK)作为丝氨酸/苏氨酸激酶家族的一个成员,是小GTP酶Rho的下游第一个效应器。ROCK接受来自于G蛋白偶联受体的信号,参与调控诸多重要的细胞活动。本文就ROCK的结构、分布、调控及生物学效应作简要介绍,并着重阐述其在缺血性脑卒中发病中的作用及其抑制剂治疗缺血性脑卒中的最新进展。 相似文献
15.
You-jiang Min Li-li-qiang Ding Li-hong Cheng Wei-ping Xiao Xing-wei He Hui Zhang Zhi-yun Min Jia Pei 《中国神经再生研究》2017,(2):276-282
Electroacupuncture is beneficial for the recovery of spinal cord injury, but the underlying mechanism is unclear. The Rho/Rho-associated kinase(ROCK) signaling pathway regulates the actin cytoskeleton by controlling the adhesive and migratory behaviors of cells that could inhibit neurite regrowth after neural injury and consequently hinder the recovery from spinal cord injury. Therefore, we hypothesized electroacupuncture could affect the Rho/ROCK signaling pathway to promote the recovery of spinal cord injury. In our experiments, the spinal cord injury in adult Sprague-Dawley rats was caused by an impact device. Those rats were subjected to electroacupuncture at Yaoyangguan(GV3), Dazhui(GV14), Zusanli(ST36) and Ciliao(BL32) and/or monosialoganglioside treatment. Behavioral scores revealed that the hindlimb motor functions improved with those treatments. Real-time quantitative polymerase chain reaction, fluorescence in situ hybridization and western blot assay showed that electroacupuncture suppressed the m RNA and protein expression of Rho-A and Rho-associated kinase Ⅱ(ROCKⅡ) of injured spinal cord. Although monosialoganglioside promoted the recovery of hindlimb motor function, monosialoganglioside did not affect the expression of Rho-A and ROCKⅡ. However, electroacupuncture combined with monosialoganglioside did not further improve the motor function or suppress the expression of Rho-A and ROCKⅡ. Our data suggested that the electroacupuncture could specifically inhibit the activation of the Rho/ROCK signaling pathway thus partially contributing to the repair of injured spinal cord. Monosialoganglioside could promote the motor function but did not suppress expression of Rho A and ROCKⅡ. There was no synergistic effect of electroacupuncture combined with monosialoganglioside. 相似文献
16.
Rho激酶(Rho-associated kirmse,ROCK)属于丝氨酸/苏氨酸蛋白激酶家族成员,是目前功能研究最为清楚的Rho下游靶效应分子,参与调节细胞的多种行为与功能,包括收缩、游走粘附、生长分裂、生存、肿瘤细胞的转化和浸润. 相似文献
17.
目的 探讨Rho激酶(Rho-associated kinase,ROCK)抑制剂法舒地尔(Fasudil)对BV2小胶质细胞极化的影响.方法 免疫荧光观察细胞形态及ROCK2表达水平;乳酸脱氢酶(Lactate dehydrogenase,LDH)细胞毒性检测试剂盒检测Fasudil对细胞的毒性作用;逆转录聚合酶链反... 相似文献
18.
背景：目前在血管新生的研究方法中，体外器官水平主要采用鸡胚绒毛尿囊膜实验模型，此方法的应用有其局限性。研究查明，Rho激酶参与血管新生，但尚缺少体外器官水平的深入观察。
目的：建立大鼠主动脉环体外培养血管新生实验模型，以Rho激酶抑制剂HA-1077为干预因素，观察Rho激酶活性抑制对血管新生的影响，以及新生血管的生长特征和规律。
设计、时间及地点：以血管环为对象，观察测量对比实验，于2008-10-21/ 2009-01-28在广东医学院生理学研究室进行。
材料：2月龄SPF级SD大鼠，雌雄不限；HA-1077 (Cat: 371970)为Calbiochem公司产品。
方法：无菌条件下取大鼠一段胸主动脉，剪为长约1 mm的血管环，随机分为对照组、HA-1077低、中、高浓度组，对照组用HG-DMEM+体积分数15%胎牛血清的培养液培养，HA-1077组分别在培养液中加入10，30，60 mmol/L HA-1077，第5天终止实验。
主要观察指标：拍摄微血管生长图像，计数体外培养的主动脉环新生微血管分支数；Western Blot检测ROCKⅠ及ROCKⅡ的表达。
结果：与对照组比较，HA-1077低浓度组新生微血管数明显增加(P < 0.01)；中、高浓度组新生微血管数较对照组明显减少(P < 0.01)。对照组和HA-1077低浓度组都有ROCKⅠ和ROCKⅡ表达，组间比较差异无显著性意义；HA-1077中、高浓度组则基本未见ROCKⅠ或ROCKⅡ表达。
结论：30，60 mmol/L HA-1077可以抑制血管新生，并抑制Rho激酶表达。提示Rho激酶抑制可以减少体外培养大鼠主动脉环的血管新生。 相似文献
19.
近年来研究表明,他汀类药物有防治阿尔茨海默病(AD)的作用,但机制尚不明确。诸多研究证明他汀类药物可通过降脂作用或抑制异戊二烯化阻断Rho蛋白信号转导通路,增强α分泌酶活性,减少Aβ淀粉样蛋白的产生。本文综述了他汀类药物及Rho/ROCK途径与AD的关系,探索了他汀类药物通过Rho激酶抑制途径,影响Aβ前体蛋白(APP)代谢,发挥其对AD防治作用的机制。 相似文献
20.
《中国神经再生研究》2016,(6):983-987
Spontaneous axonal regeneration of neurons does not occur after spinal cord injury because of inhibition by myelin and other inhibitory factors. Studies have demonstrated that blocking the Rho/Rho-kinase (ROCK) pathway can promote neurite outgrowth in spinal cord injury models. In the present study, we investigated neurite outgrowth and neuronal differentiation in neural stem cells from the mouse subventricular zone after inhibition of ROCK in vitro. Inhibition of ROCK with Y-27632 increased neurite length, enhanced neuronal differentiation, and upregulated the expression of two major signaling pathway effectors, phospho-Akt and phospho-mitogen-activated protein kinase, and the Hippo pathway effector YAP. These results suggest that inhibition of ROCK mediates neurite outgrowth in neural stem cells by activating the Hippo signaling pathway. 相似文献