You Position: Home > Paper
Serum exosomes of rats with hepatic ischemia-reperfusion injury induce the damage of hippocampus and cerebral cortex
( views:21, downloads:0 )
- Author:
- No author available
- Journal Title:
- Acta Physiologica Sinica
- Issue:
- 4
- DOI:
- 10.13294/j.aps.2020.0044
- Key Word:
- 外泌体;缺血再灌注;肝;海马;大脑皮质
Abstract： 本文旨在探究大鼠肝缺血再灌注(ischemia/reperfusion,I/R)后血清中外泌体的变化及其在海马和大脑皮质损伤中的作用.采用随机数字表法将清洁级雄性Sprague-Dawley (SD)大鼠分为4组:假手术组(S组)、肝缺血再灌注组(I/R组)、S组大鼠血清外泌体处理组(ES组)和I/R组大鼠血清外泌体处理组(EI组).ES组和EI组为正常大鼠经尾静脉分别注射S组和I/R组大鼠血清中的外泌体各100 μL.另取3只正常大鼠经尾静脉注射PKH26红色荧光标记的外泌体,利用免疫荧光显微镜观察大鼠脑组织中荧光表达情况.应用透射电子显微镜观察外泌体的形态和大小:免疫蛋白印迹法检测外泌体标记蛋白CD63和CD9的表达情况;通过血清学和组织学指标的检测,观察肝及脑组织损伤情况及海马和大脑皮质组织细胞凋亡和氧化应激水平.结果 显示:外泌体是直径为30～100 nm的圆形或椭圆形膜性囊泡.与S组比较,I/R组大鼠血清中外泌体含量增加(P＜0.05).外泌体具有血脑屏障通透性,可自外周经血液循环进入脑组织.I/R组血清肝功能指标较S组明显升高(P＜0.05).与S组比较,ES组脑组织损伤程度及海马和大脑皮质组织细胞凋亡和氧化应激水平无显著变化;与S组、ES组比较,I/R组、EI组血清脑损伤标志物水平、海马和大脑皮质组织中凋亡指数、氧化应激水平升高,但EI组以上指标均低于I/R组(P＜0.05).因此,大鼠肝I/R可导致海马和大脑皮质组织损伤,而且其介导的血清外泌体含量增加在其中发挥了重要作用.
- [1]María Pascual,Francesc Ibá(n)ez,Consuelo Guerri.Exosomes as mediators of neuron-glia communication in neuroinflammation[J].2020,(5).
- [2]Anuradha Kalani,Neetu Tyagi.Exosomes in neurological disease, neuroprotection, repair and therapeutics: problems and perspectives[J].2015,(10).
- [3]Jiliang Shen,Chiung-Kuei Huang,Hong Yu,etc.The role of exosomes in hepatitis, liver cirrhosis and hepatocellular carcinoma[J].2017,21(5).
- [4]Jing Jing, Li,Bin, Wang,Mahesh Chandra, Kodali,etc.In vivo evidence for the contribution of peripheral circulating inflammatory exosomes to neuroinflammation.[J].2018,15(1).
- [5]Yang Mu‐qing,Du Qiang,Goswami Julie,etc.Interferon regulatory factor 1-Rab27a regulated extracellular vesicles promote liver ischemia/reperfusion injury[J].2018,67(3).
- [6]Zoraida, Andreu,María, Yá?ez-Mó.Tetraspanins in extracellular vesicle formation and function.[J].2014,5.
- [7]Jia Lili,Wang Fei,Gu Xiangqian,etc.Propofol postconditioning attenuates hippocampus ischemia-reperfusion injury via modulating JAK2/STAT3 pathway in rats after autogenous orthotropic liver transplantation[J].2017,1657.
- [8]Rivest S.Molecular insights on the cerebral innate immune system.[J].2003,17(1).
- [9]Emre S,Miller CM,Boccagni P,etc.Central nervous system complications in liver transplant recipients--incidence, timing, and long-term follow-up.[J].2000,14(1).
- [10]Kalani,A.,Tyagi,A.,Tyagi,N..Exosomes: Mediators of neurodegeneration, neuroprotection and therapeutics[J].2014,49(1).
- [11]Kathryn M, Lenz,Lars H, Nelson.Microglia and Beyond: Innate Immune Cells As Regulators of Brain Development and Behavioral Function.[J].2018,9(Spec ).
- [12]Zhai,Y.,Petrowsky,H.,Hong,J.C.,etc.Ischaemia-reperfusion injury in liver transplantation-from bench to bedside[J].2013,10(2).
- [13]Archana, Gupta,Lynn, Pulliam.Exosomes as mediators of neuroinflammation.[J].2014,11.
- [14]Yanfeng,Gao,Shuang,Zhou,Fengfei,Wang,etc.Hepatoprotective effects of limb ischemic post-conditioning in hepatic ischemic rat model and liver cancer patients via PI3K/ERK pathways.[J].2018,14(14).
- [15]Stammet,P.,Wagner,D.R.,Gilson,G.,etc.Modeling serum level of s100β and bispectral index to predict outcome after cardiac arrest[J].2013,62(9).
- [16]Hadi Valadi,Karin Ekstrom,Apostolos Bossios,etc.Exosome-mediated transfer of mRNAs and microRNAs is a novel mechanism of genetic exchange between cells[J].2007,9(6).
- [17]D. M. Pegtel,L. Peferoen,S. Amor.Extracellular vesicles as modulators of cell-to-cell communication in the healthy and diseased brain[J].2014,369(1652).
- [18]Xiangyang,Yu,Lili,Jia,Kuoqi,Yin,etc.Src is Implicated in Hepatic Ischemia Reperfusion-Induced Hippocampus Injury and Long-Term Cognitive Impairment in Young Mice via NMDA Receptor Subunit 2A Activation.[J].2018,391.
- [19]Papageorgiou, Ismini E.,Lewen, Andrea,Galow, Lukas V.,etc.TLR4-activated microglia require IFN-gamma to induce severe neuronal dysfunction and death in situ[J].2016,113(1).