活性氧调控巨噬细胞极化的研究进展
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摘要
巨噬细胞可以极化为两种表型:经典激活巨噬细胞(M1)和替代激活巨噬细胞(M2),前者分泌促炎细胞因子来促进炎性反应,而后者分泌炎性抑制因子抑制过量炎性反应、促进血管生成、组织修复和肿瘤生长等。作为重要的第二信使,活性氧(ROS)不仅导致促炎细胞因子的产生,而且促进肿瘤的发生和发展。在不同刺激条件下,ROS可调控巨噬细胞的极化过程,使其向不同表型转换,从而发挥不同作用。
Macrophages are divided into classically( M1) and alternatively( M2) activated macrophage phenotypes. The former secretes pro-inflammatory cytokines to amplify inflammation,while the latter secretes inflammation inhibition factors to inhibit excessive inflammation and promote angiogenesis,tissue repair,tumor growth and so on. As an important second messenger reactive oxygen species( ROS) not only leads to the production of proinflammatory cytokines,but also promotes the occurrence and development of cancer.Under different stimulating conditions,ROS can transform macrophage into different phenotypes by regulating the polarization process,and further play different roles.
Macrophages are divided into classically( M1) and alternatively( M2) activated macrophage phenotypes. The former secretes pro-inflammatory cytokines to amplify inflammation,while the latter secretes inflammation inhibition factors to inhibit excessive inflammation and promote angiogenesis,tissue repair,tumor growth and so on. As an important second messenger reactive oxygen species( ROS) not only leads to the production of proinflammatory cytokines,but also promotes the occurrence and development of cancer.Under different stimulating conditions,ROS can transform macrophage into different phenotypes by regulating the polarization process,and further play different roles.
引文
[1]Guidarelli A,Fiorani M,Cerioni L,et al.Arsenite induces DNA damage via mitochondrial ROS and induction of mitochondrial permeability transition[J].Biofactors,2017,43:673-684.
[2]Hafner C,Wu J,Soto-Gonzalez L,et al.Moderate hyperoxia induces inflammation,apoptosis and necrosis in human umbilical vein endothelial cells:An in-vitro study[J].Eur J Anaesthesiol,2017,34:141-149.
[3]Yang YF,Zhou YD,Hu JC,et al.Ficolin-A/2,acting as a new regulator of macrophage polarization,mediates the inflammatory response in experimental mouse colitis[J].Immunology,2017,151:433-450.
[4]Lee HW,Lee CG,Rhee DK,et al.Sinigrin inhibits production of inflammatory mediators by suppressing NF-kappa B/MAPK pathways or NLRP3 inflammasome activation in macrophages[J].Int Immunopharmacol,2017,45:163-173.
[5]Zhang Q,Deng Y,Lai W,et al.Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation[J].Sci Rep,2016,6:30146.10.1038/srep30146.
[6]Lee HH,Lee SG,Shin JS,et al.p-Coumaroyl antho-cyanin mixture isolated from tuber epidermis of solanum tuberosum attenuates reactive oxygen species and pro-inflammatory mediators by suppressing NF-kappaB and STAT1/3 signaling in LPS-induced RAW264.7 macrophages[J].Biol Pharm Bull,2017,40:1894-1902.
[7]Zhao Q,Chen H,Yang T,et al.Direct effects of airborne PM2.5 exposure on macrophage polarizations[J].Biochim Biophys Acta,2016,1860:2835-2843.
[8]Qi S,Feng Z,Li Q,et al.Myricitrin modulates NADPHoxidase-dependent ROS production to inhibit endotoxinmediated inflammation by blocking the JAK/STAT1 and NOX2/p47phox pathways[J].Oxid Med Cell Longev,2017,2017:9738745.10.1155/2017/9738745
[9]Beceiro S,Radin J N,Chatuvedi R,et al.TRPM2 ion channels regulate macrophage polarization and gastric inflammation during Helicobacter pylori infection[J].Mucosal Immunol,2017,10:493-507.
[10]Mudaliar H,Rayner B,Billah M,et al.Remote ischemic preconditioning attenuates EGR-1 expression following myocardial ischemia reperfusion injury through activation of the JAK-STAT pathway[J].Int J Cardiol,2017,228:729-741.
[11]Gan ZS,Wang QQ,Li JH,et al.Iron reduces M1 macrophage polarization in RAW264.7 macrophages associated with inhibition of STAT1[J].Mediators Inflamm,2017,2017:8570818.10.1155/2017/8570818.
[12]Meyer A,Laverny G,Allenbach Y,et al.IFN-beta-induced reactive oxygen species and mitochondrial damage contribute to muscle impairment and inflammation maintenance in dermatomyositis[J].Acta Neuropathol,2017,134:655-666.
[13]Orsolic N,Kunstic M,Kukolj M,et al.Oxidative stress,polarization of macrophages and tumour angiogenesis:Efficacy of caffeic acid[J].Chem Biol Interact,2016,256:111-124.
[14]Zhang Y,Choksi S,Chen K,et al.ROS play a critical role in the differentiation of alternatively activated macrophages and the occurrence of tumor-associated macrophages[J].Cell Res,2013,23:898-914.
[15]Cui J,Xu W,Chen J,et al.M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung epithelial cells[J].Oncotarget,2017,8:21398-21409.
[16]Gnanaprakasam J,Estrada-Muniz E,Vega L.The anacardic 6-pentadecyl salicylic acid induces macrophage activation via the phosphorylation of ERK1/2,JNK,P38 kinases and NF-kappaB[J].Int Immunopharmacol,2015,29:808-817.
[17]Kang H,Zhang J,Wang B,et al.Puerarin inhibits M2polarization and metastasis of tumor-associated macro-phages from NSCLC xenograft model via inactivating MEK/ERK 1/2 pathway[J].Int J Oncol,2017,50:545-554.
[18]Shan M,Qin J,Jin F,et al.Autophagy suppresses isoprenaline-induced M2 macrophage polarization via the ROS/ERK and m TOR signaling pathway[J].Free Radic Biol Med,2017,110:432-443.
[19]Ho VW,Hofs E,Elisia I,et al.All trans retinoic acid,transforming growth factor beta and prostaglandin E2 in mouse plasma synergize with basophil-secreted interleukin-4 to M2 polarize murine macrophages[J].PLoSOne,2016,11:e168072.doi:10.1371/journal.pone.0168072.
[20]Nagaraj C,Haitchi HM,Heinemann A,et al.Increased expression of p22phox mediates airway hyperresponsiveness in an experimental model of asthma[J].Antioxid Redox Signal,2017,27:1460-1472.
[21]He C,Larson-Casey JL,Gu L,et al.Cu,Zn-superoxide dismutase-mediated redox regulation of jumonji domain containing 3 modulates macrophage polarization and pulmonary fibrosis[J].Am J Respir Cell Mol Biol,2016,55:58-71.
[2]Hafner C,Wu J,Soto-Gonzalez L,et al.Moderate hyperoxia induces inflammation,apoptosis and necrosis in human umbilical vein endothelial cells:An in-vitro study[J].Eur J Anaesthesiol,2017,34:141-149.
[3]Yang YF,Zhou YD,Hu JC,et al.Ficolin-A/2,acting as a new regulator of macrophage polarization,mediates the inflammatory response in experimental mouse colitis[J].Immunology,2017,151:433-450.
[4]Lee HW,Lee CG,Rhee DK,et al.Sinigrin inhibits production of inflammatory mediators by suppressing NF-kappa B/MAPK pathways or NLRP3 inflammasome activation in macrophages[J].Int Immunopharmacol,2017,45:163-173.
[5]Zhang Q,Deng Y,Lai W,et al.Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation[J].Sci Rep,2016,6:30146.10.1038/srep30146.
[6]Lee HH,Lee SG,Shin JS,et al.p-Coumaroyl antho-cyanin mixture isolated from tuber epidermis of solanum tuberosum attenuates reactive oxygen species and pro-inflammatory mediators by suppressing NF-kappaB and STAT1/3 signaling in LPS-induced RAW264.7 macrophages[J].Biol Pharm Bull,2017,40:1894-1902.
[7]Zhao Q,Chen H,Yang T,et al.Direct effects of airborne PM2.5 exposure on macrophage polarizations[J].Biochim Biophys Acta,2016,1860:2835-2843.
[8]Qi S,Feng Z,Li Q,et al.Myricitrin modulates NADPHoxidase-dependent ROS production to inhibit endotoxinmediated inflammation by blocking the JAK/STAT1 and NOX2/p47phox pathways[J].Oxid Med Cell Longev,2017,2017:9738745.10.1155/2017/9738745
[9]Beceiro S,Radin J N,Chatuvedi R,et al.TRPM2 ion channels regulate macrophage polarization and gastric inflammation during Helicobacter pylori infection[J].Mucosal Immunol,2017,10:493-507.
[10]Mudaliar H,Rayner B,Billah M,et al.Remote ischemic preconditioning attenuates EGR-1 expression following myocardial ischemia reperfusion injury through activation of the JAK-STAT pathway[J].Int J Cardiol,2017,228:729-741.
[11]Gan ZS,Wang QQ,Li JH,et al.Iron reduces M1 macrophage polarization in RAW264.7 macrophages associated with inhibition of STAT1[J].Mediators Inflamm,2017,2017:8570818.10.1155/2017/8570818.
[12]Meyer A,Laverny G,Allenbach Y,et al.IFN-beta-induced reactive oxygen species and mitochondrial damage contribute to muscle impairment and inflammation maintenance in dermatomyositis[J].Acta Neuropathol,2017,134:655-666.
[13]Orsolic N,Kunstic M,Kukolj M,et al.Oxidative stress,polarization of macrophages and tumour angiogenesis:Efficacy of caffeic acid[J].Chem Biol Interact,2016,256:111-124.
[14]Zhang Y,Choksi S,Chen K,et al.ROS play a critical role in the differentiation of alternatively activated macrophages and the occurrence of tumor-associated macrophages[J].Cell Res,2013,23:898-914.
[15]Cui J,Xu W,Chen J,et al.M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung epithelial cells[J].Oncotarget,2017,8:21398-21409.
[16]Gnanaprakasam J,Estrada-Muniz E,Vega L.The anacardic 6-pentadecyl salicylic acid induces macrophage activation via the phosphorylation of ERK1/2,JNK,P38 kinases and NF-kappaB[J].Int Immunopharmacol,2015,29:808-817.
[17]Kang H,Zhang J,Wang B,et al.Puerarin inhibits M2polarization and metastasis of tumor-associated macro-phages from NSCLC xenograft model via inactivating MEK/ERK 1/2 pathway[J].Int J Oncol,2017,50:545-554.
[18]Shan M,Qin J,Jin F,et al.Autophagy suppresses isoprenaline-induced M2 macrophage polarization via the ROS/ERK and m TOR signaling pathway[J].Free Radic Biol Med,2017,110:432-443.
[19]Ho VW,Hofs E,Elisia I,et al.All trans retinoic acid,transforming growth factor beta and prostaglandin E2 in mouse plasma synergize with basophil-secreted interleukin-4 to M2 polarize murine macrophages[J].PLoSOne,2016,11:e168072.doi:10.1371/journal.pone.0168072.
[20]Nagaraj C,Haitchi HM,Heinemann A,et al.Increased expression of p22phox mediates airway hyperresponsiveness in an experimental model of asthma[J].Antioxid Redox Signal,2017,27:1460-1472.
[21]He C,Larson-Casey JL,Gu L,et al.Cu,Zn-superoxide dismutase-mediated redox regulation of jumonji domain containing 3 modulates macrophage polarization and pulmonary fibrosis[J].Am J Respir Cell Mol Biol,2016,55:58-71.