高迁移率族蛋白B1与肝缺血再灌注损伤的关系
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摘要
高迁移率族蛋白B1(HMGB1)是一种广泛分布于真核细胞中的DNA结合蛋白。当组织损伤时,HMGB1作为内源性危险信号激活机体免疫系统,介导无菌炎症反应。目前已发现其在肝脏缺血再灌注损伤中发挥关键作用。归纳了近年HMGB1在肝缺血再灌注中如何发挥促炎作用以及以HMGB1为靶点治疗肝缺血再灌注损伤的研究进展。
High-mobility group box B1( HMGB1) is a DNA-binding protein widely distributed in eukaryotic cells. When tissue damageoccurs,HMGB1 acts as an endogenous risk signal to activate the body's immune system and mediate aseptic inflammatory response. Currentresearch findings have shown that HMGB1 plays a key role in hepatic ischemia-reperfusion injury. This article summarizes the recent re-search advances in the proinflammatory role of HMGB1 in hepatic ischemia-reperfusion and HMGB1 as a target for the treatment of hepaticischemia-reperfusion injury.
High-mobility group box B1( HMGB1) is a DNA-binding protein widely distributed in eukaryotic cells. When tissue damageoccurs,HMGB1 acts as an endogenous risk signal to activate the body's immune system and mediate aseptic inflammatory response. Currentresearch findings have shown that HMGB1 plays a key role in hepatic ischemia-reperfusion injury. This article summarizes the recent re-search advances in the proinflammatory role of HMGB1 in hepatic ischemia-reperfusion and HMGB1 as a target for the treatment of hepaticischemia-reperfusion injury.
引文
[1] EKANAYAKA SA,MCCLELLAN SA,PENG XD,et al. HMGB1antagonist,box A,reduces TLR4,RAGE,and inflammatorycytokines in the cornea of P. aeruginosa-infected mice[J]. JOcul Pharmacol Ther,2018,34(10):1-9.
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[3] YANG H,WANG H,JU Z,et al. MD-2 is required for disul-fide HMGB1-dependent TLR4 signaling[J]. J Exp Med,2015,212(1):5-14.
[4] YANG H,LUNDBCK P,OTTOSSON L,et al. Redox modifi-cation of cysteine residues regulates the cytokine activity ofhigh mobility group box-1(HMGB1)[J]. Mol Med,2016,18(1):250-259.
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[7] HAO N,BUDNIK BA,GUNAWARDENA J,et al. Tunable sig-nal processing through modular control of transcription factortranslocation[J]. Science,2013,339(6118):460-464.
[8] ZHOU H,JIN C,CUI L,et al. HMGB1 contributes to the irra-diation-induced endothelial barrier injury through receptor foradvanced glycation endproducts(RAGE)[J]. J Cell Physiol,2018,233(9):6714-6721.
[9] SUNG PH,LEE FY,LIN LC,et al. Melatonin attenuated braindeath tissue extract-induced cardiac damage by suppressingDAMP signaling[J]. Oncotarget,2018,9(3):3531-3548.
[10] MIHM S. Danger-associated molecular patterns(DAMPs):Molecular triggers for sterile inflammation in the liver[J]. Int JMol Sci,2018,19(10):1-12.
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[13] LIU A,DIRSCH O,FANG H,et al. HMGB1 translocation andexpression is caused by warm ischemia reperfusion injury,butnot by partial hepatectomy in rats[J]. Exp Mol Pathol,2011,91(2):502-508.
[14] LIU A,DIRSCH O,FANG H,et al. HMGB1 in ischemic andnon-ischemic liver after selective warm ischemia/reperfusionin rat[J]. Histochem Cell Biol,2011,135(5):443-452.
[15] CANNISTRM,RUGGIERO M,ZULLO A,et al. Hepatic is-chemia reperfusion injury:A systematic review of literature andthe role of current drugs and biomarkers[J]. Int J Surg,2016,33(Suppl 1):s57-s70.
[16] CUI Z,LI S,LIU Z,et al. Interferon regulatory factor 1 acti-vates autophagy to aggravate hepatic ischemia-reperfusioninjury by increasing high mobility group box 1 release[J]. CellPhysiol Biochem,2018,48(1):328-338.
[17] ZHU JR,LU HD,GUO CH,et al. Berberine attenuates ische-mia-reperfusion injury through inhibiting HMGB1 release andNF-κB nuclear translocation[J]. Acta Pharmacol Sin,2018,39(11):1706-1715.
[18] WU K,ZHANG H,FU Y,et al. TLR4/MyD88 signaling deter-mines the metastatic potential of breast cancer cells[J]. MolMed Rep,2018,18(3):3411-3420.
[19] CHEN BH,LI WM. Effect of ulinastatin combined with ische-mic preconditioning on hepatic ischemia-reperfusion injury inrats[J]. J Clin Hepatol,2018,34(2):369-372.(in Chi-nese)陈宝鹤,李文美.乌司他丁联合缺血预处理对大鼠肝缺血再灌注损伤的影响[J].临床肝胆病杂志,2018,34(2):369-372.
[20] SHAKER ME,TRAWICK BN,MEHAL WZ. The novel TLR9 an-tagonist COV08-0064 protects from ischemia/reperfusion in-jury in non-steatotic and steatotic mice livers[J]. BiochemPharmacol,2016,112:90-101.
[21] HUANG H,NACE GW,MCDONALD KA,et al. Hepatocyte-specific high-mobility group box 1 deletion worsens the injuryin liver ischemia/reperfusion:A role for intracellular high-mobility group box 1 in cellular protection[J]. Hepatology,2014,59(5):1984-1997.
[22] TSAROUCHA AK,VALSAMI G,KOSTOMITSOPOULOS N,etal. Silibinin effect on Fas/FasL,HMGB1,and CD45 expres-sions in a rat model subjected to liver ischemia-reperfusioninjury[J]. J Invest Surg,2017:1-12.
[23] LI X,WU Y,ZHANG W,et al. Pre-conditioning with tanshi-none IIA attenuates the ischemia/reperfusion injury caused byliver grafts via regulation of HMGB1 in rat Kupffer cells[J]. Bi-omed Pharmacother,2017,89:1392-1400.
[24] TONG Y,TANG Z,YANG T,et al. Ulinastatin preconditioningattenuates inflammatory reaction of hepatic ischemia reperfu-sion injury in rats via high mobility group box 1(HMGB1)inhi-bition[J]. Int J Med Sci,2014,11(4):337-343.
[25] YANG H,OCHANI M,LI J,et al. Reversing established sep-sis with antagonists of endogenous high-mobility group box 1[J]. Proc Natl Acad Sci U S A,2004,101(1):296-301.
[26] YAMAMOTO T,ONO T,ITO T,et al. Hemoperfusion with ahigh-mobility group box 1 adsorption column can prevent theoccurrence of hepatic ischemia-reperfusion injury in rats[J].Crit Care Med,2010,38(3):879-888.
[2] LU B,NAKAMURA T,INOUYE K,et al. Novel role of PKR ininflammasome activation and HMGB1 release[J]. Nature,2012,488(7413):670-674.
[3] YANG H,WANG H,JU Z,et al. MD-2 is required for disul-fide HMGB1-dependent TLR4 signaling[J]. J Exp Med,2015,212(1):5-14.
[4] YANG H,LUNDBCK P,OTTOSSON L,et al. Redox modifi-cation of cysteine residues regulates the cytokine activity ofhigh mobility group box-1(HMGB1)[J]. Mol Med,2016,18(1):250-259.
[5] TANG D,KANG R,ZEH HJ,et al. High-mobility group box1,oxidative stress,and disease[J]. Antioxid Redox Signal,2011,14(7):1315-1335.
[6] TANG D,KANG R,LIVESEY KM,et al. Endogenous HMGB1regulates autophagy[J]. J Cell Biol,2010,190(5):881-892.
[7] HAO N,BUDNIK BA,GUNAWARDENA J,et al. Tunable sig-nal processing through modular control of transcription factortranslocation[J]. Science,2013,339(6118):460-464.
[8] ZHOU H,JIN C,CUI L,et al. HMGB1 contributes to the irra-diation-induced endothelial barrier injury through receptor foradvanced glycation endproducts(RAGE)[J]. J Cell Physiol,2018,233(9):6714-6721.
[9] SUNG PH,LEE FY,LIN LC,et al. Melatonin attenuated braindeath tissue extract-induced cardiac damage by suppressingDAMP signaling[J]. Oncotarget,2018,9(3):3531-3548.
[10] MIHM S. Danger-associated molecular patterns(DAMPs):Molecular triggers for sterile inflammation in the liver[J]. Int JMol Sci,2018,19(10):1-12.
[11] LV WL,ARNESANO F,CARLONI P,et al. Effect of in vivopost-translational modifications of the HMGB1 protein uponbinding to platinated DNA:A molecular simulation study[J].Nucleic Acids Res,2018,46(22):11687-11697.
[12] VENEREAU E,DE LF,MEZZAPELLE R,et al. HMGB1 as bio-marker and drug target[J]. Pharmacol Res,2016,111:534-544.
[13] LIU A,DIRSCH O,FANG H,et al. HMGB1 translocation andexpression is caused by warm ischemia reperfusion injury,butnot by partial hepatectomy in rats[J]. Exp Mol Pathol,2011,91(2):502-508.
[14] LIU A,DIRSCH O,FANG H,et al. HMGB1 in ischemic andnon-ischemic liver after selective warm ischemia/reperfusionin rat[J]. Histochem Cell Biol,2011,135(5):443-452.
[15] CANNISTRM,RUGGIERO M,ZULLO A,et al. Hepatic is-chemia reperfusion injury:A systematic review of literature andthe role of current drugs and biomarkers[J]. Int J Surg,2016,33(Suppl 1):s57-s70.
[16] CUI Z,LI S,LIU Z,et al. Interferon regulatory factor 1 acti-vates autophagy to aggravate hepatic ischemia-reperfusioninjury by increasing high mobility group box 1 release[J]. CellPhysiol Biochem,2018,48(1):328-338.
[17] ZHU JR,LU HD,GUO CH,et al. Berberine attenuates ische-mia-reperfusion injury through inhibiting HMGB1 release andNF-κB nuclear translocation[J]. Acta Pharmacol Sin,2018,39(11):1706-1715.
[18] WU K,ZHANG H,FU Y,et al. TLR4/MyD88 signaling deter-mines the metastatic potential of breast cancer cells[J]. MolMed Rep,2018,18(3):3411-3420.
[19] CHEN BH,LI WM. Effect of ulinastatin combined with ische-mic preconditioning on hepatic ischemia-reperfusion injury inrats[J]. J Clin Hepatol,2018,34(2):369-372.(in Chi-nese)陈宝鹤,李文美.乌司他丁联合缺血预处理对大鼠肝缺血再灌注损伤的影响[J].临床肝胆病杂志,2018,34(2):369-372.
[20] SHAKER ME,TRAWICK BN,MEHAL WZ. The novel TLR9 an-tagonist COV08-0064 protects from ischemia/reperfusion in-jury in non-steatotic and steatotic mice livers[J]. BiochemPharmacol,2016,112:90-101.
[21] HUANG H,NACE GW,MCDONALD KA,et al. Hepatocyte-specific high-mobility group box 1 deletion worsens the injuryin liver ischemia/reperfusion:A role for intracellular high-mobility group box 1 in cellular protection[J]. Hepatology,2014,59(5):1984-1997.
[22] TSAROUCHA AK,VALSAMI G,KOSTOMITSOPOULOS N,etal. Silibinin effect on Fas/FasL,HMGB1,and CD45 expres-sions in a rat model subjected to liver ischemia-reperfusioninjury[J]. J Invest Surg,2017:1-12.
[23] LI X,WU Y,ZHANG W,et al. Pre-conditioning with tanshi-none IIA attenuates the ischemia/reperfusion injury caused byliver grafts via regulation of HMGB1 in rat Kupffer cells[J]. Bi-omed Pharmacother,2017,89:1392-1400.
[24] TONG Y,TANG Z,YANG T,et al. Ulinastatin preconditioningattenuates inflammatory reaction of hepatic ischemia reperfu-sion injury in rats via high mobility group box 1(HMGB1)inhi-bition[J]. Int J Med Sci,2014,11(4):337-343.
[25] YANG H,OCHANI M,LI J,et al. Reversing established sep-sis with antagonists of endogenous high-mobility group box 1[J]. Proc Natl Acad Sci U S A,2004,101(1):296-301.
[26] YAMAMOTO T,ONO T,ITO T,et al. Hemoperfusion with ahigh-mobility group box 1 adsorption column can prevent theoccurrence of hepatic ischemia-reperfusion injury in rats[J].Crit Care Med,2010,38(3):879-888.