巨噬细胞极化与动脉粥样硬化相关性及中药干预作用研究进展
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摘要
综述巨噬细胞极化与动脉粥样硬化的相关性及中药干预作用的研究进展。M1型巨噬细胞极化可以促进动脉粥样硬化的发展,而M2型巨噬细胞极化对动脉粥样硬化的发展起到双重作用;丹参、穿心莲、姜黄、肉桂、黄连等中药的提取物,可以通过调节巨噬细胞极化,起到控制动脉粥样硬化进程的作用。
This paper reviews the relationship between macrophage polarization and atherosclerosis and the intervention effects of traditional Chinese medicine. M1 type macrophage polarization can promote the development of atherosclerosis, while M2 type macrophage polarization plays a dual role on atherosclerosis. The extracts of traditional Chinese medicine such as Danshen(Radix SalviaeMiltiorrhizae), Chuɑnxinlian(HerbaAnorographitis), Jianghuang(RhizomaCurcumaeLongae), Guipi(Cortex CinnamomiJaponici), Huɑnglian(RhizomaCoptidis)can control the progression of atherosclerosis by regulating the polarization of macrophages.
This paper reviews the relationship between macrophage polarization and atherosclerosis and the intervention effects of traditional Chinese medicine. M1 type macrophage polarization can promote the development of atherosclerosis, while M2 type macrophage polarization plays a dual role on atherosclerosis. The extracts of traditional Chinese medicine such as Danshen(Radix SalviaeMiltiorrhizae), Chuɑnxinlian(HerbaAnorographitis), Jianghuang(RhizomaCurcumaeLongae), Guipi(Cortex CinnamomiJaponici), Huɑnglian(RhizomaCoptidis)can control the progression of atherosclerosis by regulating the polarization of macrophages.
引文
[1]陆二梅,李益星,白杨,等.巨噬细胞极化的研究进展[J].现代生物医学进展,2016,16(32):6397-400.
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[3]LAWRENCE T,NATOLI G.Transcriptional regulation of macrophage polarization:enabling diversity with identity[J].Nat Rev Immunol,2011,11(11):750-761.
[4]HUANG W C,SALA-NEWBY G B,SUSANA A,et al.Classical macrophage activation up-regulates several matrix metalloproteinases through mitogen activated protein kinases and nuclear factor-kappaB[J].PLoS One,2012,7(8):e42507.
[5]ZHANG B,MA Y,XIANG C.SIRT2 decreases atherosclerotic plaque formation in low-density lipoprotein receptor-deficient mice by modulating macrophage polarization[J].Biomed Pharmacother,2018(97):1238-1242.
[6]DERLINDATI E,DEI C A,MONTANINI B,et al.Transcriptomic analysis of human polarized macrophages:more than one role of alternative activation?[J].PLoS One,2015,10(3):e0119751.
[7]郑新,王红艳.M2型巨噬细胞极化及相关疾病的研究进展[J].生命科学,2017,29(9):883-890.
[8]EI C C,SCHWARZFISCHER L,REHLI M.Interleukin-4 induced interferon regulatory factor(Irf)4 participates in the regulation of alternative macrophage priming[J].Immunobiology,2010,215(9-10):821-825.
[9]董蓉.调控巨噬细胞M2型极化的长链非编码RNA发现及小分子化合物的干预研究[D].杭州:浙江大学,2017.
[10]ISA S A,RUFFINO J S,AHLUWALIA M,et al.M2 macrophages exhibit higher sensitivity to ox LDL-induced lipotoxicity than other monocyte/macrophage subtypes[J].Lipids Health Dis,2011(10):229.
[11]OH J,RIEK A E,WENG S,et al.Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation[J].J Biol Chem,2012,287(15):11629-11641.
[12]白瑞娜,郗瑞席,冯志博,等.巨噬细胞与动脉粥样硬化---亚型及功能[J].中国循环杂志,2014,29(5):393-395.
[13]袁锋,尚茹茹,张锦,等.巨噬细胞极化与动脉粥样硬化[J].中华临床医师杂志(电子版),2015,9(22):4176-4179.
[14]周冰冰,李玉洁,李琦,等.参莲提取物对M1巨噬细胞的影响[J].中国中药杂志,2014,39(11):2086-2090.
[15]温洁霞.基于炎性体研究丹参酮ⅡA抗动脉粥样硬化的分子机制[D].石家庄:河北农业大学,2014.
[16]陈方圆,袁祖贻,周娟,等.姜黄素促进RAW264.7源性M1巨噬细胞向替代激活M2表型极化[J].西安交通大学学报(医学版),2015,36(2):257-262.
[17]姜涛,王剑.桂皮醛对LPS诱导的Raw264.7巨噬细胞迁移和M1极化的抑制作用研究[J].中药新药与临床药理,2016,27(3):361-365.
[18]王洪杰.黄连抑制LPS诱导的小鼠巨噬细胞MCP-1合成的机制研究[D].武汉:华中科技大学,2011.
[19]陈博,万敬员.小檗碱对氧化型低密度脂蛋白诱导巨噬细胞促炎细胞因子和活性氧的影响[J].中华中医药学刊,2017,35(11):2752-2755.
[20]明康文,洪创雄,姜涛,等.淫羊藿苷联合齐墩果酸对RAW264.7小鼠巨噬细胞迁移和M1极化的影响[J].广州中医药大学学报,2016,33(3):366-371.
[21]马莉娜.五甲基槲皮素对脂多糖诱导的小鼠巨噬细胞系RAW264.抗炎作用的研究[D].武汉:华中科技大学,2009.
[22]刘佳.左旋箭毒碱、异粒枝碱和轮环藤碱对巨噬细胞过度活化的抑制作用及机制研究[D].沈阳:辽宁大学,2017.
[23]刘敏.表没食子儿茶素没食子酸酯对白介素-4诱导的小鼠M2型巨噬细胞标志性因子表达的影响[D].郑州:河南师范大学,2016.
[24]曾海燕,方勇,曾高峰.丹红注射液对脂多糖诱导THP-1巨噬细胞促炎因子分泌的影响及机制[J].中南医学科学杂志,2014,42(5):443-446.
[25]张衡.葛根素抑制ox LDL诱导的巨噬细胞激活和泡沫细胞形成[D].锦州:锦州医科大学,2016.
[26]黄靓,熊文昊,王汉群,等.鬼箭羽水溶成分抑制氧化型低密度蛋白诱导的THP-1源性巨噬细胞炎症因子表达[J].中国现代药物应用,2014,8(14):250-251.
[27]李冬方,顾宁,黄伟.黄芪多糖对THP-1巨噬细胞HSP60诱导下IL-6、TNF-α表达的影响[J].时珍国医国药,2015,26(12):2830-2832.
[28]ZHANG X,LIU M H,QIAO L,et al.Ginsenoside Rb1 enhances atherosclerotic plaque stability by skewing macrophages to the M2phenotype[J].J Cell Mol Med,2018,22(1):409-416.
[29]HYAM S R,LEE I A,GU W,et al.Arctigenin ameliorates inflammation in vitro and in vivo by inhibiting the PI3K/AKT pathway and polarizing M1 macrophages to M2-like macrophages[J].Eur J Pharmacol,2013,708(1-3):21-29.
[30]刘卓,隋海娟,闫恩志,等.知母皂苷对脂多糖引起巨噬细胞分泌TNF-α和NO的影响及机制[J].中药药理与临床,2013,29(1):65-67.
[31]潘德锋.木犀草素通过PI3K/Akt途径调节巨噬细胞表型转化抑制凋亡的机制研究[D].南京:南京中医药大学,2017.
[32]杨迎飞.红景天苷调节巨噬细胞极化抗动脉粥样硬化的实验研究[D].昆明:云南中医学院,2018.
[2]吴秀华,郑文洁.巨噬细胞极化[J].中华临床免疫和变态反应杂志,2017,11(2):161-165.
[3]LAWRENCE T,NATOLI G.Transcriptional regulation of macrophage polarization:enabling diversity with identity[J].Nat Rev Immunol,2011,11(11):750-761.
[4]HUANG W C,SALA-NEWBY G B,SUSANA A,et al.Classical macrophage activation up-regulates several matrix metalloproteinases through mitogen activated protein kinases and nuclear factor-kappaB[J].PLoS One,2012,7(8):e42507.
[5]ZHANG B,MA Y,XIANG C.SIRT2 decreases atherosclerotic plaque formation in low-density lipoprotein receptor-deficient mice by modulating macrophage polarization[J].Biomed Pharmacother,2018(97):1238-1242.
[6]DERLINDATI E,DEI C A,MONTANINI B,et al.Transcriptomic analysis of human polarized macrophages:more than one role of alternative activation?[J].PLoS One,2015,10(3):e0119751.
[7]郑新,王红艳.M2型巨噬细胞极化及相关疾病的研究进展[J].生命科学,2017,29(9):883-890.
[8]EI C C,SCHWARZFISCHER L,REHLI M.Interleukin-4 induced interferon regulatory factor(Irf)4 participates in the regulation of alternative macrophage priming[J].Immunobiology,2010,215(9-10):821-825.
[9]董蓉.调控巨噬细胞M2型极化的长链非编码RNA发现及小分子化合物的干预研究[D].杭州:浙江大学,2017.
[10]ISA S A,RUFFINO J S,AHLUWALIA M,et al.M2 macrophages exhibit higher sensitivity to ox LDL-induced lipotoxicity than other monocyte/macrophage subtypes[J].Lipids Health Dis,2011(10):229.
[11]OH J,RIEK A E,WENG S,et al.Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation[J].J Biol Chem,2012,287(15):11629-11641.
[12]白瑞娜,郗瑞席,冯志博,等.巨噬细胞与动脉粥样硬化---亚型及功能[J].中国循环杂志,2014,29(5):393-395.
[13]袁锋,尚茹茹,张锦,等.巨噬细胞极化与动脉粥样硬化[J].中华临床医师杂志(电子版),2015,9(22):4176-4179.
[14]周冰冰,李玉洁,李琦,等.参莲提取物对M1巨噬细胞的影响[J].中国中药杂志,2014,39(11):2086-2090.
[15]温洁霞.基于炎性体研究丹参酮ⅡA抗动脉粥样硬化的分子机制[D].石家庄:河北农业大学,2014.
[16]陈方圆,袁祖贻,周娟,等.姜黄素促进RAW264.7源性M1巨噬细胞向替代激活M2表型极化[J].西安交通大学学报(医学版),2015,36(2):257-262.
[17]姜涛,王剑.桂皮醛对LPS诱导的Raw264.7巨噬细胞迁移和M1极化的抑制作用研究[J].中药新药与临床药理,2016,27(3):361-365.
[18]王洪杰.黄连抑制LPS诱导的小鼠巨噬细胞MCP-1合成的机制研究[D].武汉:华中科技大学,2011.
[19]陈博,万敬员.小檗碱对氧化型低密度脂蛋白诱导巨噬细胞促炎细胞因子和活性氧的影响[J].中华中医药学刊,2017,35(11):2752-2755.
[20]明康文,洪创雄,姜涛,等.淫羊藿苷联合齐墩果酸对RAW264.7小鼠巨噬细胞迁移和M1极化的影响[J].广州中医药大学学报,2016,33(3):366-371.
[21]马莉娜.五甲基槲皮素对脂多糖诱导的小鼠巨噬细胞系RAW264.抗炎作用的研究[D].武汉:华中科技大学,2009.
[22]刘佳.左旋箭毒碱、异粒枝碱和轮环藤碱对巨噬细胞过度活化的抑制作用及机制研究[D].沈阳:辽宁大学,2017.
[23]刘敏.表没食子儿茶素没食子酸酯对白介素-4诱导的小鼠M2型巨噬细胞标志性因子表达的影响[D].郑州:河南师范大学,2016.
[24]曾海燕,方勇,曾高峰.丹红注射液对脂多糖诱导THP-1巨噬细胞促炎因子分泌的影响及机制[J].中南医学科学杂志,2014,42(5):443-446.
[25]张衡.葛根素抑制ox LDL诱导的巨噬细胞激活和泡沫细胞形成[D].锦州:锦州医科大学,2016.
[26]黄靓,熊文昊,王汉群,等.鬼箭羽水溶成分抑制氧化型低密度蛋白诱导的THP-1源性巨噬细胞炎症因子表达[J].中国现代药物应用,2014,8(14):250-251.
[27]李冬方,顾宁,黄伟.黄芪多糖对THP-1巨噬细胞HSP60诱导下IL-6、TNF-α表达的影响[J].时珍国医国药,2015,26(12):2830-2832.
[28]ZHANG X,LIU M H,QIAO L,et al.Ginsenoside Rb1 enhances atherosclerotic plaque stability by skewing macrophages to the M2phenotype[J].J Cell Mol Med,2018,22(1):409-416.
[29]HYAM S R,LEE I A,GU W,et al.Arctigenin ameliorates inflammation in vitro and in vivo by inhibiting the PI3K/AKT pathway and polarizing M1 macrophages to M2-like macrophages[J].Eur J Pharmacol,2013,708(1-3):21-29.
[30]刘卓,隋海娟,闫恩志,等.知母皂苷对脂多糖引起巨噬细胞分泌TNF-α和NO的影响及机制[J].中药药理与临床,2013,29(1):65-67.
[31]潘德锋.木犀草素通过PI3K/Akt途径调节巨噬细胞表型转化抑制凋亡的机制研究[D].南京:南京中医药大学,2017.
[32]杨迎飞.红景天苷调节巨噬细胞极化抗动脉粥样硬化的实验研究[D].昆明:云南中医学院,2018.