• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肢体缺血后处理对短暂性脑缺血大鼠行为改善及神经细胞增殖的影响

[Effects of Limb Ischemic Postconditioning on Behavioral Improvement and Proliferation of Neural Cells in Rats with Transient Cerebral Ischemia].

作者信息

Huang Dan, Liu Hong-Hong, Yang Zhen, Qu Yun

机构信息

Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu 610041, China.

Key Laboratory of Rehabilitation Medicine, Sichuan University, Chengdu 610041, China.

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2017 May;48(3):378-383.

PMID:28616910
Abstract

OBJECTIVES

To determine the effects of non-invasive limb ischemic postconditioning (NLIP) on the behavioral performance and the expression and distribution of neural cells in rats with ischemic cortex.

METHODS

Rats were randomly divided into 3 groups: sham group (=10), ischemia/reperfusion (I/R) group (=50), and NLIP group (=50). Focal cerebral ischemia was induced by intraluminal MCAO in the rats in the I/R and NLIP groups, while no suture was inserted in the sham-operated rats. NLIP (reperfusion-10 min, ischemia-10 min, ×3 cycles) was conducted immediately after reperfusion on bilateral femoral arteries by modified ischemicelastic bands. Body mass and behavioral performance of the rats were assessed at 3 d, 7 d, 14 d, 21 d and 28 d post-ischemia (=5-10). Doublecortin (DCX) and glial fibrillary acidic protein (GFAP) in the ischemic cortex were detected by immunohistochemistry.The expression of microtubule associated protein 2 (MAP2) was detected by Western blot.

RESULTS

The rats in the sham group showed mild body mass loss and minor neurological deficit 1-3 d post-ischemia and weakened muscle strength 1 d post-ischemia, which were alleviated gradually overtime. Compared with the sham group, neurological deficits were more obvious in the rats in the I/R and NLIP groups, which were alleviated 3-21 d post-ischemia and reached a level close to that of the sham group at 28 d post-ischemia. No significant difference was found betweenthe I/R and NLIP groups in neurologic deficit scores.NLIP significantly alleviated body mass loss 2-7 d post-ischemia (<0.05) and improved muscle strength 14-28 d post-ischemia (<0.05).Compared with the sham group, rats in the I/R and NLP groups had increased numbers of DCX and GFAP-labeled cells in the ischemic penumbra over time, increased hypotrophic cell bodies and longer and thickened dendrites, and decreased expression of MAP2 (>0.05) at 3 d post-ischemia prior to an up-regulation.Higher expression of MAP2 was found 14-21 d post-ischemia (<0.05) in the I/R group and 7-28 d post-ischemia in the NLIP group(<0.05). Significant difference in MAP2 was found between the I/R and NLIP groups at 7 d post-ischemia (<0.05).

CONCLUSIONS

NLIP has the potential to improve neurological outcomes and promote increase of neural cells in penumbral cortex after cerebral ischemia.

摘要

目的

确定非侵入性肢体缺血后处理(NLIP)对缺血性皮质大鼠行为表现以及神经细胞表达和分布的影响。

方法

将大鼠随机分为3组:假手术组(n = 10)、缺血/再灌注(I/R)组(n = 50)和NLIP组(n = 50)。I/R组和NLIP组大鼠通过大脑中动脉线栓法诱导局灶性脑缺血,假手术组大鼠不插入线栓。NLIP(再灌注10分钟,缺血10分钟,共3个循环)在再灌注后立即通过改良的缺血弹性带对双侧股动脉进行处理。在缺血后3天、7天、14天、21天和28天评估大鼠的体重和行为表现(每组n = 5 - 10)。通过免疫组织化学检测缺血皮质中的双皮质素(DCX)和胶质纤维酸性蛋白(GFAP)。通过蛋白质免疫印迹法检测微管相关蛋白2(MAP2)的表达。

结果

假手术组大鼠在缺血后1 - 3天体重轻度下降,有轻微神经功能缺损,缺血后1天肌肉力量减弱,随着时间推移逐渐缓解。与假手术组相比,I/R组和NLIP组大鼠的神经功能缺损更明显,在缺血后3 - 21天缓解,在缺血后28天达到接近假手术组的水平。I/R组和NLIP组在神经功能缺损评分上无显著差异。NLIP显著减轻缺血后2 - 7天的体重下降(P<0.05),并改善缺血后14 - 28天的肌肉力量(P<0.05)。与假手术组相比,I/R组和NLIP组大鼠缺血半暗带中DCX和GFAP标记细胞数量随时间增加,细胞体萎缩、树突变长变粗,缺血后3天MAP2表达降低(P>0.05),之后上调。I/R组在缺血后14 - 21天MAP2表达较高(P<0.05),NLIP组在缺血后7 - 28天MAP2表达较高(P<0.05)。缺血后7天I/R组和NLIP组MAP2表达有显著差异(P<0.05)。

结论

NLIP有改善神经功能结局并促进脑缺血后半暗带皮质神经细胞增加的潜力。

相似文献

1
[Effects of Limb Ischemic Postconditioning on Behavioral Improvement and Proliferation of Neural Cells in Rats with Transient Cerebral Ischemia].肢体缺血后处理对短暂性脑缺血大鼠行为改善及神经细胞增殖的影响
Sichuan Da Xue Xue Bao Yi Xue Ban. 2017 May;48(3):378-383.
2
[Effects of combined ischemic postconditioning, remote ischemic postconditioning and naloxone postconditioning on focal cerebral ischemia-reperfusion injury in rats].[联合缺血后处理、远程缺血后处理及纳洛酮后处理对大鼠局灶性脑缺血再灌注损伤的影响]
Zhonghua Yi Xue Za Zhi. 2011 Jun 7;91(21):1493-7.
3
[Effects of electroacupuncture preconditioning on expression of nitric oxide synthase and glial fibrillary acidic protein in cortex of focal cerebral ischemia-reperfusion rats].[电针预处理对局灶性脑缺血再灌注大鼠皮层一氧化氮合酶及胶质纤维酸性蛋白表达的影响]
Zhen Ci Yan Jiu. 2015 Apr;40(2):113-8.
4
The role of p38MAPK signal pathway in the neuroprotective mechanism of limb postconditioning against rat cerebral ischemia/reperfusion injury.p38丝裂原活化蛋白激酶信号通路在肢体后处理对大鼠脑缺血/再灌注损伤神经保护机制中的作用。
J Neurol Sci. 2015 Oct 15;357(1-2):270-5. doi: 10.1016/j.jns.2015.08.004. Epub 2015 Aug 5.
5
Role of mitophagy regulated by Parkin/DJ-1 in remote ischemic postconditioning-induced mitigation of focal cerebral ischemia-reperfusion.由帕金蛋白/ DJ-1调控的线粒体自噬在远隔缺血后处理减轻局灶性脑缺血再灌注损伤中的作用
Eur Rev Med Pharmacol Sci. 2015 Dec;19(24):4866-71.
6
Transforming growth-beta 1 contributes to isoflurane postconditioning against cerebral ischemia-reperfusion injury by regulating the c-Jun N-terminal kinase signaling pathway.转化生长因子-β1通过调节c-Jun氨基末端激酶信号通路,有助于异氟烷对脑缺血再灌注损伤的后处理作用。
Biomed Pharmacother. 2016 Mar;78:280-290. doi: 10.1016/j.biopha.2016.01.030. Epub 2016 Feb 4.
7
[Effect of transcutaneous auricular vagus nerve stimulation on the expressions of GFAP and MAP2 in ischemic penumbra of rats with middle cerebral artery ischemia].[经皮耳迷走神经刺激对大脑中动脉缺血大鼠缺血半暗带中GFAP和MAP2表达的影响]
Zhen Ci Yan Jiu. 2022 Jan 25;47(1):33-8. doi: 10.13702/j.1000-0607.20210059.
8
Wnt/β-catenin signaling pathway contributes to isoflurane postconditioning against cerebral ischemia-reperfusion injury and is possibly related to the transforming growth factorβ1/Smad3 signaling pathway.Wnt/β-catenin 信号通路有助于异氟醚后处理对脑缺血再灌注损伤的保护作用,其可能与转化生长因子β1/Smad3 信号通路有关。
Biomed Pharmacother. 2019 Feb;110:420-430. doi: 10.1016/j.biopha.2018.11.143. Epub 2018 Dec 5.
9
Remote ischemic post-conditioning improves neurological function by AQP4 down-regulation in astrocytes.远程缺血后处理通过下调星形胶质细胞中的水通道蛋白4来改善神经功能。
Behav Brain Res. 2015 Aug 1;289:1-8. doi: 10.1016/j.bbr.2015.04.024. Epub 2015 Apr 21.
10
Remote ischemic postconditioning protects the brain from focal ischemia/reperfusion injury by inhibiting autophagy through the mTOR/p70S6K pathway.远程缺血后适应通过mTOR/p70S6K通路抑制自噬,从而保护大脑免受局灶性缺血/再灌注损伤。
Neurol Res. 2018 Mar;40(3):182-188. doi: 10.1080/01616412.2018.1424696. Epub 2018 Jan 25.