内毒素休克引起多器官损伤发病机制研究进展
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摘要
内毒素休克引起的多器官损伤是导致患者死亡的重要原因。一方面,内毒素活化多条信号通路作用于炎性细胞,促使细胞因子和黏附因子分泌,导致全身炎症反应失控;另一方面,内毒素作用于血管内皮细胞、中性粒细胞,引起血管反应性降低、通透性增加、血液流变性异常,导致微循环障碍。从炎症反应与微循环障碍两方面综述了内毒素休克引起多器官损伤的发病机制,为防治内毒素性休克提供新思路。
引文
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[39] SONG J W,ZULLO J A,LIVERIS D,et al.Therapeutic restoration of endothelial glycocalyx in sepsis[J].J Pharmacol Exp Ther,2017,361(1):115-121.
[40] WANG X Q,ZHANG Y P,ZHANG L M,et al.Resveratrol enhances vascular reactivity in mice following lipopolysaccharide challenge via the RhoA-ROCK-MLCP pathway[J].Exp Ther Med,2017,14(1):308-316.
[41] WANG Y,CUI H,NIU F,et al.Effect of resveratrol on blood rheological properties in LPS-challenged rats[J].Front Physiol,2018,29(9):1202.
[2] CHO W H.Update of sepsis:recent evidences about early goal-directed therapy[J].Tuberc Respir Dis(Seoul),2015,78(3):156-160.
[3] VAEZ H,NAJAFI M,TOUTOUNCHI N S,et al.Metformin alleviates lipopolysaccharide-induced acute lung injury through suppressing toll-like receptor 4 signaling [J].Iran J Allergy Asthma Immunol,2016,15(6):498-507.
[4] NOGUEIRA-MACHADO J A,De OLIVEIRA VOLPE C M.HMGB-1 as a target for inflammation controlling[J].Recent Pat Endocr Metab Immune Drug Discov,2012,6(3):201-209.
[5] KIM J H,KIM S J,LEE I S,et al.Bacterial endotoxin induces the release of high mobility group Box 1 via the IFN-β signaling pathway[J].J Immunol,2009,18(2):2458-2466.
[6] SCAFFIDI P,MISTELI T,BIANCHI M E.Release of chromatin protein HMGB-1 by necrotic cells triggers inflammation[J].Nature,2002,41(8):191-195.
[7] BRET J,SCHMIDT A M,YAN S D,et al.Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues[J].Am J Pathol,1993,143(6):1699-1712.
[8] 彭伟.晚期糖化终产物受体在树突状细胞及T淋巴细胞免疫中的作用[J].国际内科学杂志,2009,36(12):689-692.
[9] LIN L.RAGE on the Toll road[J].Cell Mol Immuno1,2006,3(5):351-358.
[10] NEEPER M,SCHMIDT A M,BRETT J,et al.Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins[J].J Biol Chem,1992,267(21):14998-15004.
[11] YANG Z Y,LING Y,YIN T,et al.Delayed ethyl pyruvate therapy attenuates experimental severe acute pancreatitis via reduced serum high mobility group Box 1 levels in rats[J].World J Gastroenterol,2008,14(28):4546-4550.
[12] CHENG B Q,LIU C T,LI W J,et al.Ethyl pyruvate improves survival and ameliorates distant organ injury in rats with severe acute pancreatitis[J].Pancreas,2007,35(3):256-261.
[13] SAPPINGTON P L,YANG R,YANG H,et al.HMGB-1 increases the permeability of Caco-2 enterocytic monolayers and impairs intestinal barrier function in mice [J].Gastroenterology,2002,123(3):790-802.
[14] YANG R,TENHUNEN J,TONNESSEN T I.HMGB-1 and histones play a significant role in inducing systemic inflammation and multiple organ dysfunctions in severe acute pancreatitis[J].Int J Inflam,2017,2017:1817564.
[15] VENEREAU E,De LEO F,MEZZAPELLE R,et al.HMGB-1 as biomarker and drug target[J].Pharmacol Res,2016,111:534-544.
[16] YAN S F,YAN S D,RAMASAMY R,et al.Tempering the wrath of RAGE:an emerging therapeutic strategy against diabetic complications,neurodegeneration,and inflammation [J].Ann Med,2009,41(6):408-422.
[17] KIERDORF K,FRITZ G.RAGE regulation and signaling in inflammation and beyond[J].J Leukocyte Biol,2013,94(1):55-68.
[18] LI J,SCHMIDT A M.Characterization and functional analysis of the promoter of RAGE,the receptor for advanced glycation end products[J].J Biol Chem,1997,272(26):16498-16506.
[19] NOGUEIRA-MACHADO J A,VOLPE C M,VELOSO C A,et al.HMGB1,TLR and RAGE:a functional tripod that leads to diabetic inflammation[J].Expert Opin Ther Targets,2011,15(8):1023-1035.
[20] YEH C H,STURGIS L,HAIDACHER J,et al.Requirement for p38 and p44/p42 mitogen-activated protein kinases in RAGE-mediated nuclear factor-kappaB transcriptional activation and cytokine secretion[J].Diabetes,2001,50(6):1495-1504.
[21] 刘瑛.Amphoterin-RAGE轴与肿瘤[J].美国中华临床医学杂志,2004,6(3):270-273.
[22] 赵善超,侯凡凡,姜勇.晚期糖基化终产物受体的结构和功能[J].生理科学进展,2003,34(1):71-73.
[23] ZHANG Z,ZHOU J,LIAO C,et al.RAGE deficiency attenuates the protective effect of lidocaine against sepsis-induced acute lung injury[J].Inflammation,2017,40(2):601-611.
[24] TEMIZ-RESITOGLU M,KUCUKKAVRUK S P,GUDEN D S,et al.Activation of mTOR/IκB-α/NF-κB pathway contributes to LPS-induced hypotension and inflammation in rats[J].Eur J Pharmacol,2017,802:7-19.
[25] INCE C.The microcirculation is the motor of sepsis[J].Crit Care,2005,9(4):S13.
[26] 李彤,田牛,罗毅.组织通道研究[J].微循环学杂志,2012,22(2):1-5.
[27] DELLINGER R P,LEVY M M,RHODES A,et al.Surviving sepsis campaign:international guidelines for management of severe sepsis and septic shock[J].Int Care Med,2013,39(2):165-228.
[28] SUZUKI T,SUZUKI Y,OKUDA J,et al.Sepsis-induced cardiac dysfunction and β-adrenergic blockade therapy for sepsis[J].J Int Care,2017,5(1):22.
[29] BOISRAME-HELMS J,KREMER H,SCHINI-KERTH V,et al.Endothelial dysfunction in sepsis[J].Curr Vasc Pharmacol,2013,11(2):150-160.
[30] GANDO S.Role of fibrinolysis in sepsis[J].Semin Thromb Hemost,2013,39(4):392-399.
[31] LUSH C W,KVIETYS P R.Microvascular dysfunction in sepsis[J].Microcirculation,2000,7(2):83-101.
[32] PARK S Y,SHRESTHA S,YOUN Y J,et al.Autophagy primes neutrophils for neutrophil extracellular trap formation during sepsis[J].Am J Respir Crit Care Med,2017,196(5):577-589.
[33] YU L,DA X,WU X,et al.Simvastatin prevents lipopolysaccharide-induced septic shock in rats[J].J Huazhong Univ Sci Technolog Med Sci,2017,37(2):226-230.
[34] SHI W L,ZHANG T,ZHOU J R,et al.Rapid permissive action of dexamethasone on the regulation of blood pressure in a rat model of septic shock[J].Biomed Pharmacother,2016,84:1119-1125.
[35] BOZ M,ATILLA P,ISKIT A B,et al.Effects of ATP-sensitive potassium channel blockers on vascular hyporeactivity,mesenteric blood flow,and survival in lipopolysaccharide-induced septic shock model[J].Can J Physiol Pharmacol,2016,94(8):858-867.
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[37] DUAN C Y,ZHANG J,WU H L,et al.Regulatory mechanisms,prophylaxis and treatment of vascular leakage following severe trauma and shock[J].Mil Med Res,2017,4(1):11.
[38] WANG L,WU J,GUO X,et al.RAGE plays a role in LPS-induced NF-κB activation and endothelial hyperpermeability[J].Sensors,2017,17(4):722.
[39] SONG J W,ZULLO J A,LIVERIS D,et al.Therapeutic restoration of endothelial glycocalyx in sepsis[J].J Pharmacol Exp Ther,2017,361(1):115-121.
[40] WANG X Q,ZHANG Y P,ZHANG L M,et al.Resveratrol enhances vascular reactivity in mice following lipopolysaccharide challenge via the RhoA-ROCK-MLCP pathway[J].Exp Ther Med,2017,14(1):308-316.
[41] WANG Y,CUI H,NIU F,et al.Effect of resveratrol on blood rheological properties in LPS-challenged rats[J].Front Physiol,2018,29(9):1202.