[1]何霜霜,朱娱,周赫男,等.周细胞对失血性休克大鼠血管通透性的保护作用[J].第三军医大学学报,2020,42(19):1882-1889.
 HE Shuangshuang,ZHU Yu,ZHOU Henan,et al.Protective effect of pericytes against vascular leakage in rats with hemorrhagic shock[J].J Third Mil Med Univ,2020,42(19):1882-1889.
点击复制

周细胞对失血性休克大鼠血管通透性的保护作用(/HTML )
分享到:

《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
42卷
期数:
2020年第19期
页码:
1882-1889
栏目:
军事医学
出版日期:
2020-10-15

文章信息/Info

Title:
Protective effect of pericytes against vascular leakage in rats with hemorrhagic shock
作者:
何霜霜朱娱周赫男王洪晨李涛刘良明
陆军军医大学(第三军医大学)野战外科研究所战伤休克与输血研究室,创伤、烧伤与复合伤国家重点实验室
Author(s):
HE Shuangshuang ZHU Yu ZHOU Henan WANG Hongchen LI Tao LIU Liangming
State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, 400042, China
 
关键词:
周细胞失血性休克血管通透性ZO-1VE-cadherin
Keywords:
pericytes hemorrhagic shock vascular permeability zonula occludens 1 VE-cadherin
分类号:
R322.12;R329.27;R605.971
文献标志码:
A
摘要:

目的探讨周细胞(pericyte, PC)对失血性休克(hemorrhagic shock, HS)大鼠血管渗漏的保护作用。方法采用失血性休克(血压30 mmHg,维持3 h)模型,将12~24周龄SD大鼠(雌雄各半,体质量200~220 g)分成4组(n=16):假手术组(Sham组)、失血性休克组(HS组)、乳酸林格氏液治疗组(LR组)、PC治疗组(PC组),治疗组在失血性休克大鼠血压至30 mmHg,维持3 h后开始治疗,治疗12 h后取材,观察不同处理组大鼠肺静脉上的周细胞数量、肺血管及肠系膜微血管的通透性、内皮紧密连接ZO-1和黏附连接VE-cadherin的表达变化。结果与正常对照组相比,失血性休克大鼠血管渗漏明显加重(P<0.05),周细胞数量减少,内皮细胞超微结构紧密连接破坏,内皮细胞间紧密连接ZO-1和黏附连接VE-cadherin的表达明显降低(P<0.05)。LR治疗12 h后能够轻微降低失血性休克大鼠的血管通透性;紧密连接开放程度轻微降低,内皮细胞间紧密连接ZO-1和黏附连接VE-cadherin的表达轻微升高。与LR组相比,PC治疗12 h后,失血性休克大鼠肺静脉上周细胞数量增加;细胞形态恢复,超微结构紧密连接开放程度显著降低;内皮细胞间紧密连接ZO-1和黏附连接VE-cadherin的表达明显著升高(P<0.05),恢复至接近正常水平;血管渗漏明显改善,肠系膜微血管通透性显著降低。结论周细胞对失血性休克大鼠血管渗漏具有明显的保护作用。

Abstract:

ObjectiveTo investigate the protective effect of pericytes (PCs) against vascular leakage in rats with hemorrhagic shock. MethodsSixty-four 12- to 24-week-old SD rats weighing 200~220 g were randomized equally into sham-operated group, hemorrhagic shock group (HS group), Ringer’s lactate solution treatment group (LR group), and PC treatment group (PC group). In the latter 3 groups, rat models of hemorrhagic shock were established by lowering the blood pressure to 30 mmHg, which was maintained for 3 h. Tissue samples were collected 12 h after corresponding treatment for determination of the number of pericytes, vascular permeability of the pulmonary vessels and the mesenteric microvessels, and expressions of zonula occludens 1 (ZO-1) and VE-cadherin. ResultsThe vascular permeability was increased (P<0.05) and the number of pericytes and expressions of ZO-1 and VE-cadherin were decreased significantly (P<0.05) in rats with hemorrhagic shock compared with the sham-operated rats. At 12 h after LR treatment, the vascular permeability was slightly reduced, the tight junction between the endothelial cells was moderately improved and the expression levels of ZO-1 and VE-cadherin were mildly increased in rats with hemorrhagic shock. At 12 h after PC treatment, the number of pericytes in the pulmonary vein was increased, the cell morphology and tight junction between the endothelial cells were restored, and the expressions of ZO-1 and VE-cadherin were increased significantly to nearly the normal levels in rats with hemorrhagic shock (P<0.05); the mesenteric microvascular permeability and vascular leakage were improved significantly after treatment with PCs. ConclusionPC infusion produces significantly protective effect against vascular leakage in rats with hemorrhagic shock. 

参考文献/References:

[1]HUA T F, YANG M, ZHOU Y Y, et al. Alda-1 prevents pulmonary epithelial barrier dysfunction following severe hemorrhagic shock through clearance of reactive aldehydes[J]. Biomed Res Int, 2019, 2019: 2476252. DOI: 10.1155/2019/2476252. 
[2]MA Q Y, ZHAO Z, SAGARE A P, et al. Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism[J]. Mol Neurodegener, 2018, 13: 57. DOI: 10.1186/s13024-018-0286-0. 
[3]ZONNEVILLE J, SAFINA A, TRUSKINOVSKY A M, et al. TGF-β signaling promotes tumor vasculature by enhancing the pericyte-endothelium association[J]. BMC Cancer, 2018, 18(1): 670. DOI: 10.1186/s12885-018-4587-z. 
[4]SHIMIZU F, SANO Y, SAITO K, et al. Pericyte-derived glial cell line-derived neurotrophic factor increase the expression of claudin-5 in the blood-brain barrier and the blood-nerve barrier[J]. Neurochem Res, 2012, 37(2): 401-409. DOI: 10.1007/s11064-011-0626-8. 
[5]TACHIBANA M, YAMAZAKI Y, LIU C C, et al. Pericyte implantation in the brain enhances cerebral blood flow and reduces amyloid-β pathology in amyloid model mice[J]. Exp Neurol, 2018, 300: 13-21. DOI: 10.1016/j.expneurol.2017.10.023. 
[6]BELL R D, WINKLER E A, SAGARE A P, et al. Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging[J]. Neuron, 2010, 68(3): 409-427. DOI: 10.1016/j.neuron.2010.09.043. 
[7]DURHAM J T, DULMOVITS B M, CRONK S M, et al. Pericyte chemomechanics and the angiogenic switch: insights into the pathogenesis of proliferative diabetic retinopathy?[J]. Investig Ophthalmol Vis Sci, 2015, 56(6): 3441-3459. DOI: 10.1167/iovs.14-13945. 
[8]MCGUIRE P G, RANGASAMY S, MAESTAS J, et al. Pericyte-derived sphinogosine 1-phosphate induces the expression of adhesion proteins and modulates the retinal endothelial cell barrier[J]. Arterioscler Thromb Vasc Biol, 2011, 31(12): 107-115. DOI: 10.1161/atvbaha.111.235408. 
[9]ZHU Y, WU H L, WU Y, et al. Beneficial effect of intermedin 1-53 in septic shock rats: contributions of rho kinase and BKCA pathway-mediated improvement in cardiac function[J]. Shock Augusta Ga, 2016, 46(5): 557-565. DOI: 10.1097/SHK.0000000000000639. 
[10]CHEN C W, OKADA M, PROTO J D, et al. Human pericytes for ischemic heart repair[J]. Stem Cells, 2013, 31(2): 305-316. DOI: 10.1002/stem.1285. 
[11]MENDEL T A, CLABOUGH E B D, KAO D S, et al. Pericytes derived from adipose-derived stem cells protect against retinal vasculopathy[J]. PLoS ONE, 2013, 8(5): e65691. DOI: 10.1371/journal.pone.0065691. 
[12]TACHIBANA M, YAMAZAKI Y, LIU C C, et al. Pericyte implantation in the brain enhances cerebral blood flow and reduces amyloid-β pathology in amyloid model mice[J]. Exp Neurol, 2018, 300: 13-21. DOI: 10.1016/j.expneurol.2017.10.023. 
[13]张紫森,刘良明.周细胞对脓毒症大鼠血管反应性的保护作用[J].第三军医大学学报,2019,41(21):2029-2034. DOI: 10.16016/j.1000-5404.201907039. 
ZHANG Z S, LIU L M. Role of pericyte in protecting the vascular reactivity in septic shock rats and its mechanism [J]. J Third Mil Med Univ, 2019, 41(21): 2029-2034. DOI: 10.16016/j.1000-5404.201907039. 
[14]STARK K, ECKART A, HAIDARI S, et al. Capillary and arteriolar pericytes attract innate leukocytes exiting through venules and ‘instruct’ them with pattern-recognition and motility programs[J]. Nat Immunol, 2013, 14(1): 41-51. DOI: 10.1038/ni.2477. 
[15]PROEBSTL D, VOISIN M B, WOODFIN A, et al. Pericytes support neutrophil subendothelial cell crawling and breaching of venular walls in vivo[J]. J Exp Med, 2012, 209(6): 1219-1234. DOI: 10.1084/jem.20111622. 
[16]ALON R, NOURSHARGH S. Learning in motion: pericytes instruct migrating innate leukocytes[J]. Nat Immunol, 2013, 14(1): 14-15. DOI: 10.1038/ni.2489. 
[17]ZHAO J L, CHEN L, SHU B, et al. Angiopoietin-1 protects the endothelial cells against advanced glycation end product injury by strengthening cell junctions and inhibiting cell apoptosis[J]. J Cell Physiol, 2015, 230(8): 1895-1905. DOI: 10.1002/jcp.24920. 
[18]BLERVAQUE L, PASSERIEUX E, POMIS P, et al. Impaired training-induced angiogenesis process with loss of pericyte-endothelium interactions is associated with an abnormal capillary remodelling in the skeletal muscle of COPD patients[J]. Respir Res, 2019, 20(1): 1-12. DOI: 10.1186/s12931-019-1240-6. 

相似文献/References:

[1]李涛,刘良明,刁有芳,等.几种不同液体复苏失血性休克大鼠的适宜量研究[J].第三军医大学学报,2008,30(03):199.
 LI Tao,LIU Liang-ming,DIAO You-fang,et al.On proper volume of different fluids for hemorrhagic shock resuscitation in rats[J].J Third Mil Med Univ,2008,30(19):199.
[2]方玉强,李涛,刘良明.精氨酸血管加压素抗失血性休克作用及其与Rho kinase的关系[J].第三军医大学学报,2008,30(13):1223.
 FANG Yu-qiang,LI Tao,LIU Liang-ming.Antishock effect of arginine vasopressin and its relationship with Rho kinase[J].J Third Mil Med Univ,2008,30(19):1223.
[3]李涛,方玉强,刘良明,等.羟乙基淀粉对失血性休克大鼠复苏效果的影响[J].第三军医大学学报,2008,30(14):1319.
 LI Tao,FANG Yu-qiang,LIU Liang-ming,et al.Effects of hydroxyethyl starch at different molecular weights on hemorrhagic shock in rats[J].J Third Mil Med Univ,2008,30(19):1319.
[4]朱乐明,董兆君.失血性休克复合氰化钠中毒对兔血清氧化应激水平的影响[J].第三军医大学学报,2006,28(05):428.
[5]李涛,刘良明,刁有芳,等.不同液体对失血性休克大鼠复苏效果的影响[J].第三军医大学学报,2009,31(06):467.
 LI Tao,LIU Liang-ming,DIAO You-fang,et al.Effects of different resuscitation fluids on hemorrhagic shock in rats[J].J Third Mil Med Univ,2009,31(19):467.
[6]徐竞,杨光明,李涛,等.缺血预适应诱导的失血性休克血管反应性和钙敏感性保护[J].第三军医大学学报,2010,32(17):1807.
 Xu Jing,Yang Guangming,Li Tao,et al.Protective effect of ischemia preconditioning on vascular reactivity and calcium sensitivity in rats after hemorrhagic shock[J].J Third Mil Med Univ,2010,32(19):1807.
[7]陈垦,刘良明.缺氧诱导因子-1α对失血性休克大鼠肠系膜上动脉血管环舒张反应性的调控作用[J].第三军医大学学报,2010,32(04):319.
 Chen Ken,Liu Liangming.Effect of hypoxia-inducible factor-1α on vascular relaxation reactivity following hemorrhagic shock in rats[J].J Third Mil Med Univ,2010,32(19):319.
[8]王海英,曾洪波,靳琼瑶,等.两种胶体用于治疗失血性休克犬对红细胞免疫功能影响的对比研究[J].第三军医大学学报,2008,30(17):1647.
 WANG Hai-ying,ZENG Hong-bo,JIN Qiong-yao,et al.Effect of two colloidal fluids on red blood cell immune function in dog model of hemorrhagic shock[J].J Third Mil Med Univ,2008,30(19):1647.
[9]贾立峰,张连阳,李勇.失血性休克复苏后CO2气腹对兔肝功能及肝血流量的影响[J].第三军医大学学报,2009,31(11):1021.
 JIA Li-feng,ZHANG Lian-yang,LI Yong.Effects of CO2 pneumoperitoneum on hepatic function and hepatic blood flow after hemorrhagic shock resuscitation in rabbits[J].J Third Mil Med Univ,2009,31(19):1021.
[10]陈方祥,滕方,廖自福,等.非控制失血性休克大鼠输液输血的研究[J].第三军医大学学报,2009,31(11):1029.
 CHEN Fang-xiang,TENG Fang,LIAO Zi-fu,et al.Resuscitation for hemorrhagic shock rats: lactated Ringer’s solution with whole blood or red blood cells[J].J Third Mil Med Univ,2009,31(19):1029.

更新日期/Last Update: 2020-10-02