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丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展

冯晶晶,  李铁军,  章越凡

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文章导航 > 药学实践与服务  > 2018 >  36(2): 108-111
冯晶晶, 李铁军, 章越凡. 丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展[J]. 药学实践与服务, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
引用本文: 冯晶晶, 李铁军, 章越凡. 丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展[J]. 药学实践与服务, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
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FENG Jingjing, LI Tiejun, ZHANG Yuefan. Progress of tanshinone ⅡA on the mechanism of inflammatory response after cerebral ischemia[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
Citation: FENG Jingjing, LI Tiejun, ZHANG Yuefan. Progress of tanshinone ⅡA on the mechanism of inflammatory response after cerebral ischemia[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
shu

丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展

doi: 10.3969/j.issn.1006-0111.2018.02.003
  • 1.

    安徽中医药大学药学院, 安徽 合肥 230012

  • 2.

    安徽中医药大学药学院, 安徽 合肥 230012;上海市浦东新区浦南医院药剂科, 上海 200125

  • 3.

    第二军医大学药学院药理学教研室, 上海 200433

基金项目: 浦东新区卫生系统重要薄弱学科建设资助（PWZbr2017-16）

Progress of tanshinone ⅡA on the mechanism of inflammatory response after cerebral ischemia

  • 1.

    School of Pharmacy, Anhui University of Chinese Medicine, Hefei 230012, China

  • 2.

    School of Pharmacy, Anhui University of Chinese Medicine, Hefei 230012, China;Department of Pharmacy, Punan Hospital of Pudong New Area, Shanghai 200125, China

  • 3.

    Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China

  • 摘要: 丹参酮ⅡA是从丹参中提取的一种菲醌类衍生物，是丹参发挥脑缺血损伤保护药理作用的主要活性成分之一。炎症在脑缺血发病机制中具有重要作用。近年来许多证据表明，免疫细胞、黏附分子、炎性介质等通过诱导或调控脑缺血时中枢神经系统内免疫应答参与发病过程。综述丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展，为丹参酮ⅡA的脑缺血保护作用机制研究提供新思路。
    Abstract: Tanshinone ⅡA is a kind of phenanthraquinone derivatives derived from Salvia miltiorrhiza, which is one of the main active components of Danshen to play the protective role of cerebral ischemic injury. Inflammation plays an important role in the pathogenesis of cerebral ischemia. In recent years, much evidence shows that immune cells, adhesion molecules, inflammatory mediators have been involved in the pathogenesis of immune response in the central nervous system through induction or regulation of cerebral ischemia. In this paper, the research progress of mechanism of inflammatory response of tanshinone ⅡA after cerebral ischemia was reviewed, which provided a new idea for the study of the protective mechanism of tanshinone ⅡA in cerebral ischemia.
  • [1] Gammon K. Neurodegenerative disease:brain windfall[J]. Nature, 2014, 515(7526):299-300.
    [2] Chen RL, Balami JS, Esiri MM, et al. Ischemic stroke in the elderly:an overview of evidence[J]. Nat Rev Neurol, 2010, 6(5):256-65.
    [3] 佟玲, 苏志强. 炎性小体在脑缺血中的作用[J]. 国际脑血管病杂志, 2017, 25(2):170-173.
    [4] Zhang F, Yan C, Wei C, et al. Vinpocetine inhibits NF-κB-dependent inflammation in acute ischemic stroke patients[J]. Transl Stroke Res, 2017.
    [5] Shang YH, Tian JF, Hou M, et al. Progress on the protective effect of compounds from natural medicines on cerebral ischemia[J]. Chin J Nat Med, 2013, 11(6):588-595.
    [6] 李德川, 鲍秀琦, 孙华,等. 丹参酮ⅡA对缺血性脑中风的神经保护作用研究进展[J]. 药学学报, 2015, 50(6):635-639.
    [7] Zhao SC, Ma LS, Chu ZH, et al. Regulation of microglial activation in stroke[J]. Acta Pharmacol Sin, 2017, 38(4):445-458.
    [8] 熊怀林, 范光碧,胡兴宇. 小胶质细胞在脑缺血中的作用[J]. 四川解剖学杂志, 2005,13(2):35-37.
    [9] Cai L, Yi XB, Yuan LB, et al. The protective effect of tanshinone ⅡA on oxygen-glucose deprivation and reperfusion injury of microglia through the NLRP3 inflammatory signaling pathway[J]. Sichuan Da Xue Xue Bao Yi Xue Ban, 2016, 47(5):660-664.
    [10] Wang Y, Yang L, Yang D. Tanshinone ⅡA rescued the impairments of primary hippocampal neurons induced by BV2 microglial over-activation[J]. Neurochem Res, 2015, 40(7):1497-1508.
    [11] 宋兆晶, 吉训明, 牛小媛,等. 脑缺血后炎性反应机制的研究进展[J].中国脑血管病杂志, 2010, 7(3):154-157.
    [12] Zhou L, Bondy SC, Jian L, et al. Tanshinone ⅡA attenuates the cerebral ischemic injury-induced increase in levels of GFAP and of caspases-3 and -8[J]. Neuroscience, 2015, 288:105-111.
    [13] Yang X, Yan J, Feng J. Treatment with tanshinone ⅡA suppresses disruption of the blood-brain barrier and reduces expression of adhesion molecules and chemokines in experimental autoimmune encephalomyelitis[J]. Eur J Pharmacol, 2016, 771:18-28.
    [14] Caso JR, Moro MA, Lorenzo P, et al. Involvement of IL-1beta in acute stress-induced worsening of cerebral ischaemia in rats[J]. Eur Neuropsychopharmacol, 2007, 17(9):600-607.
    [15] Jung JE, Kim GS, Chan PH. Neuroprotection by interleukin-6 is mediated by signal transducer and activator of transcription 3 and antioxidative signaling in ischemic stroke[J]. Stroke, 2011, 42(12):3574-3579.
    [16] Zhou L, Zhang J, Wang C, et al. Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model[J]. Int J Immunopathol Pharmacol, 2017, 30(2):123-129.
    [17] Chen Y, Wu X, Yu S, et al. Neuroprotection of tanshinone ⅡA against cerebral ischemia/reperfusion injury through inhibition of macrophage migration inhibitory factor in rats[J]. PLoS ONE, 2012, 7(6):e40165.
    [18] Huang J, Upadhyay UM, Tamargo RJ. Inflammation in stroke and focal cerebral ischemia[J]. Surg Neurol, 2006, 66(3):232-245.
    [19] Tang C, Xue H, Bai C, et al. The effects of Tanshinone ⅡA on blood-brain barrier and brain edema after transient middle cerebral artery occlusion in rats[J]. Phytomedicine, 2010, 17(14):1145-1149.
    [20] Liu P, Zhao H, Wang R, et al. MicroRNA-424 protects against focal cerebral ischemia and reperfusion injury in mice by suppressing oxidative stress[J]. Stroke, 2015, 46(2):513-519.
    [21] Davis SM, Pennypacker KR. Targeting antioxidant enzyme expression as a therapeutic strategy for ischemic stroke[J]. Neurochem Int, 2017, 107:23-32.
    [22] Greco R, Demartini C, Zanaboni AM, et al. Endothelial nitric oxide synthase inhibition triggers inflammatory responses in the brain of male rats exposed to ischemia-reperfusion injury[J]. J Neurosci Res, 2017.
    [23] del Zoppo G, Ginis I, Hallenbeck JM, et al. Inflammation and stroke:putative role for cytokines, adhesion molecules and iNOS in brain response to ischemia[J]. Brain Pathol, 2000, 10(1):95-112.
    [24] Tang C, Xue HL, Bai CL, et al. Regulation of adhesion molecules expression in TNF-α-stimulated brain microvascular endothelial cells by tanshinone ⅡA:involvement of NF-κB and ROS generation[J]. Phytother Res, 2011, 25(3):376-380.
    [25] Tuttolomondo A, Di Sciacca R, Di Raimondo D, et al. Inflammation as a therapeutic target in acute ischemic stroke treatment[J]. Curr Top Med Chem, 2009, 9(14):1240-1260.
    [26] Turner RJ, Sharp FR. Implications of MMP9 for blood brain barrier disruption and hemorrhagic transformation following ischemic stroke[J]. Front Cell Neurosci, 2016, 10:56.
    [27] Zhu Y, Tang Q, Wang G, et al. Tanshinone ⅡA protects hippocampal neuronal cells from reactive oxygen species through changes in autophagy and activation of phosphatidylinositol 3-kinase, protein kinas B, and mechanistic target of rapamycin pathways[J]. Curr Neurovasc Res, 2017, 14(2):132-140.
    [28] Wang Q, Tang XN, Yenari MA. The inflammatory response in stroke[J]. J Neuroimmunol, 2007, 184(1-2):53-68.
    [29] Dong K, Xu W, Yang J, et al. Neuroprotective effects of Tanshinone ⅡA on permanent focal cerebral ischemia in mice[J]. Phytother Res, 2009, 23(5):608-613.
    [30] Wang JG, Bondy SC, Zhou L, et al. Protective effect of tanshinone ⅡA against infarct size and increased HMGB1, NF-κB, GFAP and apoptosis consequent to transient middle cerebral artery occlusion[J]. Neurochem Res, 2014, 39(2):295-304.
    [31] Leyton-Jaimes MF, Kahn J, Israelson A. Macrophage migration inhibitory factor:A multifaceted cytokine implicated in multiple neurological diseases[J]. Exp Neurol, 2017.
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  • 收稿日期:  2017-08-24
  • 修回日期:  2017-10-11

丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展

doi: 10.3969/j.issn.1006-0111.2018.02.003
  • 1. 安徽中医药大学药学院, 安徽 合肥 230012
  • 2. 安徽中医药大学药学院, 安徽 合肥 230012;上海市浦东新区浦南医院药剂科, 上海 200125
  • 3. 第二军医大学药学院药理学教研室, 上海 200433
    • 基金项目:  浦东新区卫生系统重要薄弱学科建设资助（PWZbr2017-16）
  • 收稿日期: 2017-08-24
  • 修回日期: 2017-10-11

摘要: 丹参酮ⅡA是从丹参中提取的一种菲醌类衍生物，是丹参发挥脑缺血损伤保护药理作用的主要活性成分之一。炎症在脑缺血发病机制中具有重要作用。近年来许多证据表明，免疫细胞、黏附分子、炎性介质等通过诱导或调控脑缺血时中枢神经系统内免疫应答参与发病过程。综述丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展，为丹参酮ⅡA的脑缺血保护作用机制研究提供新思路。

English Abstract

冯晶晶, 李铁军, 章越凡. 丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展[J]. 药学实践与服务, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
引用本文: 冯晶晶, 李铁军, 章越凡. 丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展[J]. 药学实践与服务, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
shu
FENG Jingjing, LI Tiejun, ZHANG Yuefan. Progress of tanshinone ⅡA on the mechanism of inflammatory response after cerebral ischemia[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
Citation: FENG Jingjing, LI Tiejun, ZHANG Yuefan. Progress of tanshinone ⅡA on the mechanism of inflammatory response after cerebral ischemia[J]. Journal of Pharmaceutical Practice and Service, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
shu

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