血管內(nèi)皮細(xì)胞微粒在膿毒癥大鼠血管滲漏中的作用
本文選題:膿毒癥 切入點(diǎn):微粒 出處:《第三軍醫(yī)大學(xué)學(xué)報(bào)》2016年08期
【摘要】:目的探討血管內(nèi)皮細(xì)胞微粒在膿毒癥大鼠血管滲漏中的作用。方法采用盲腸結(jié)扎穿孔術(shù)(cecal ligation and puncture,CLP)復(fù)制大鼠膿毒癥模型,用流式細(xì)胞術(shù)及透射電鏡對(duì)微粒進(jìn)行鑒定,觀察膿毒癥大鼠血管滲漏變化與血液中微粒之間的關(guān)系;檢測(cè)膿毒癥大鼠來(lái)源微粒和LPS刺激肺靜脈內(nèi)皮細(xì)胞、血小板和中性粒細(xì)胞產(chǎn)生的微粒對(duì)正常大鼠和單層肺靜脈內(nèi)皮細(xì)胞通透性的影響及與緊密連接的關(guān)系。結(jié)果膿毒癥大鼠肺、腎、腸血管通透性及血液中微粒含量均隨時(shí)間顯著增加(P0.05);膿毒癥大鼠來(lái)源微粒可顯著增加正常大鼠肺、腎、腸血管通透性(P0.01)。LPS刺激血管內(nèi)皮細(xì)胞產(chǎn)生的微粒可以顯著增加正常大鼠肺血管通透性(P0.05),而LPS刺激血小板和中性粒細(xì)胞產(chǎn)生的微粒對(duì)正常大鼠肺血管通透性無(wú)明顯作用。LPS刺激血管內(nèi)皮細(xì)胞產(chǎn)生的微粒也可明顯降低單層肺靜脈內(nèi)皮細(xì)胞跨膜電阻(P0.01),降低肺靜脈內(nèi)皮細(xì)胞緊密連接ZO-1表達(dá)(P0.05)。結(jié)論內(nèi)皮細(xì)胞微?梢詤⑴c膿毒癥大鼠血管滲漏的調(diào)節(jié),其機(jī)制可能與影響血管內(nèi)皮細(xì)胞間緊密連接有關(guān)。
[Abstract]:Objective to investigate the role of vascular endothelial cell particles in vascular leakage in septic rats.Methods the sepsis model was established by cecal ligation and puncturing in rats. The microparticles were identified by flow cytometry and transmission electron microscopy. The relationship between blood vessel leakage and blood particles in septic rats was observed.The effects of particulate matter derived from sepsis and LPS stimulation on the permeability of endothelial cells of pulmonary vein, platelets and neutrophils were measured in normal and monolayer pulmonary vein endothelial cells.Results the blood vessel permeability and the content of blood particles in the lungs, kidneys and intestines of sepsis rats were significantly increased with time, while the particles derived from sepsis rats could significantly increase the lungs and kidneys of normal rats.P0.01n. LPS-stimulated microparticles produced by vascular endothelial cells significantly increased pulmonary vascular permeability in normal rats, while LPS stimulated platelet and neutrophil particles did not significantly contribute to pulmonary vascular permeability in normal rats.LPS-stimulated microparticles of vascular endothelial cells also significantly decreased the transmembrane resistance of monolayer pulmonary vein endothelial cells (P0.01A), and the expression of ZO-1 tightly connected to pulmonary vein endothelial cells (P0.05).Conclusion Endothelial microparticles may be involved in the regulation of vascular leakage in septic rats, and its mechanism may be related to the influence of tight junction between vascular endothelial cells.
【作者單位】: 第三軍醫(yī)大學(xué)大坪醫(yī)院野戰(zhàn)外科研究所第二研究室創(chuàng)傷、燒傷與復(fù)合傷國(guó)家重點(diǎn)實(shí)驗(yàn)室;
【基金】:國(guó)家自然科學(xué)基金面上項(xiàng)目(81570441)~~
【分類(lèi)號(hào)】:R459.7
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