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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

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
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

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
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

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

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
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
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