神经药理学报 ›› 2016, Vol. 6 ›› Issue (1): 41-48.DOI: 10.3969/j.issn.2095-1396.2016.01.006
王晓茹,安芳
出版日期:
2016-02-26
发布日期:
2016-05-10
通讯作者:
安芳,男,教授,硕士生导师;研究方向:中药有效成分的提取及药理活性研究;Tel:+86+0313-4029558,E-mail:wangshyh@126.com
作者简介:
王晓茹,女,硕士研究生;研究方向:中药有效成分的提取及药理活性研究;E-mail:wangxrgf@126.com
基金资助:
河北省研究生创新资助项目(No.2015-203),河北北方学院重大项目(No.ZD1314)
WANG Xiao-ru,AN Fang
Online:
2016-02-26
Published:
2016-05-10
Contact:
安芳,男,教授,硕士生导师;研究方向:中药有效成分的提取及药理活性研究;Tel:+86+0313-4029558,E-mail:wangshyh@126.com
About author:
王晓茹,女,硕士研究生;研究方向:中药有效成分的提取及药理活性研究;E-mail:wangxrgf@126.com
Supported by:
河北省研究生创新资助项目(No.2015-203),河北北方学院重大项目(No.ZD1314)
摘要: 自噬是广泛存在于真核细胞中的生命现象,它是生命体特殊的分解代谢途径,控制着细胞内蛋白质和细胞器的降解,对维持细胞生存及稳态有重要作用。现如今已成为生物医学领域的研究热点,研究发现自噬与许多疾病有关。目前,缺血性脑卒中是造成人类死亡和残疾的主要疾病之一,在治疗过程中引起的脑缺血再灌注损伤尤为普遍,受到越来越多学者的关注。该文对自噬及其在脑缺血再灌注损伤中的作用机制进行阐述,为进一步治疗缺血性脑血管疾病提供理论依据。
中图分类号:
王晓茹,安芳. 自噬及其在脑缺血再灌注损伤中作用机制[J]. 神经药理学报, 2016, 6(1): 41-48.
WANG Xiao-ru,AN Fang. Mechanism of Action of Autophagy on the Cerebral Ischemia-Reperfusion Injury[J]. Acta Neuropharmacologica, 2016, 6(1): 41-48.
[1] Knut Biber, Erik Boddeke. Neuronal CC chemokines: the distinct roles of CCL21 and CCL2 in neuropathic pain [J]. Frontiers Cell Neurosci, 2014, 8: 210.[2] Van Steenwinckel J, Reaux-Le Goazigo A, Pommier B, et al. CCL2 released from neuronal synaptic vesicles in the spinal cord is a major mediator of local inflammation and pain after peripheral nerve injury[J]. J Neurosci, 2011, 31(15): 5865-5875.[3] Moser B, Pius Loetscher. Lymphocyte traffic control by chemokines [J]. Nat Immunol, 2001, 2(2): 123-128.[4] Satish L Deshmane, Sergey Kremlev, Shohreh Amini, et al. Monocytechemoattractant protein-1 (MCP-1): an overview [J]. J Interferon & Cytokine Res, 2009, 29 (6): 313-326. [5] Marc-Andre Dansereau, Romain-Daniel Gosselin, Michel Pohl, et al. Spinal CCL2 pronociceptive action is no longer effective in CCR2 receptor antagonist-treated rats [J]. J Neurochemistry, 2008, 106(2): 757-769.[6] Michael A Thacker, Anna K Clark, Thomas Bishop, et al. CCL2 is a key mediator of microglia activation in neuropathic pain states [J]. J European Pain, 2009, 13 (3): 263-272.[7] Menetski J, Mistry S, Lu M, et al. Mice overexpressing chemokine ligand 2 (CCL2) in astrocytes display enhanced nociceptive responses [J]. Neuroscience, 2007, 149(3): 706-714.[8] Catherine Abbadie, Jill A Lindia, Anne Marie Cumiskey, et al. Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2 [J]. Science Signalling, 2003, 100(13): 7947-7952.[9] Zhang Zhi-jun, Dong Yu-lin, Lu Ying, et al. Chemokine CCL2 and its receptor CCR2 in the medullary dorsal horn are involved in trigeminal neuropathic pain [J]. J Neuroinflammation, 2012, 9(1): 136.[10] Norikazu Kiguchi, Yuka Kobayashi, Shiroh Kishioka. Chemokines and cytokines in neuroinflammation leading to neuropathic pain [J]. Current Opinion Pharmacol, 2012, 12(1): 55-61.[11] Guo Wei, Wang Hu, Zou Shi-ping, et al. Chemokine signaling involving chemokine (CC motif) ligand 2 plays a role in descending pain facilitation [J]. Neuroscience Bulletin, 2012, 21(2): 1-15.[12] Jung Hosung, Peter T Toth, Fletcher A White, et al. Monocyte chemoattractant protein‐1 functions as a neuromodulator in dorsal root ganglia neurons [J]. J Neurochemistry, 2008, 104(1): 254-263.[13] Gregory Conductier, Nicolas Blondeau, Alice Guyon, et al. The role of monocyte chemoattractant protein MCP1/CCL2 in neuroinflammatory diseases [J]. J Neuroimmunol, 2010, 224(1-2): 93-100.[14] Mounir Belkouch, Marc-Andre Dansereau, Annabelle Réaux-Le Goazigo, et al. The chemokine CCL2 increases Nav1.8 sodium channel activity in primary sensory neurons through a Gβγ -dependent mechanism [J]. J Neuroscience 2011, 31(50): 18381-18390.[15] Gao Yong-jing, Zhang Ling, Omar Abdel Samad, et al. JNK-induced MCP-1 production in spinal cord astrocytes contributes to central sensitization and neuropathic pain [J].J Neurosci, 2009, 29(13): 4096-4108.[16] Elizabeth A Old, Marzia Malcangio. Chemokine mediated neuron–glia communication and aberrant signalling in neuropathic pain states [J]. Current Opin Pharmacology, 2012, 12(1): 67-73.[17] Joachim Scholz, Clifford J Woolf. The neuropathic pain triad: neurons, immune cells and glia [J]. Nature Neuroscience, 2007, 10(11): 1361-1368.[18] Makoto Tsuda, Yukari Shigemoto-Mogami, Schuichi Koizumi, et al. P2X4 receptors induced in spinal microglia gate tactile allodynia after nerve injury [J]. Nature, 2003, 424(6950): 778-783.[19] 杜雯, 孙益. 小胶质细胞在神经病理性疼痛中的作用[J]. 细胞生物学杂志, 2007, 29(1): 11-16.[20] 高永静, 纪如荣. 星形胶质细胞调节慢性疼痛的分子机制[J]. 中国疼痛医学杂志, 2013, 19 (9): 545-552[21] Vyklicky L, Novakova-Tousova K, Benedikt J, et al. Calcium-dependent desensitization of vanilloid receptor TRPV1: a mechanism possibly involved in analgesia induced by topical application of capsaicin [J]. Physiol Res, 2008, 57(Suppl 3): S59-S68.[22] 韩重阳, 王晓良. 瞬时受体电位通道研究进展[J]. 生理科学进展, 2008, 39 (1): 27-32.[23] Michael S Gold, Gerald F Gebhart. Nociceptor sensitization in pain pathogenesis [J]. Nature Medicine, 2010, 16(11): 1248-1257.[24] Sun J H, Yang B, Donnelly D F, et al. MCP-1 enhances excitability of nociceptive neurons in chronically compressed dorsal root ganglia [J]. J Neurophysiol, 2006, 96(5): 2189-2199.[25] Der-Jang Kao, Allen H Li, Jin-Chung Chen, et al. CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons [J]. J Neuroinflammation, 2012, 9(1): 189. [26] Diana Spicarova, Pavel Adamek, Nataliia Kalynovska, et al. TRPV1 receptor inhibition decreases CCL2-induced hyperalgesia [J]. Neuropharmacology, 2014, 81: 75-84.[27] Der-Jang Kao, Alien H Li, Jin-Chung Chen, et al. CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons [J]. Journal of Neuroinflammation, 2012, 9 (1): 189. (与25条重复)[28] Han Ying, Li Yan, Xiao Xing, et al. Formaldehyde up-regulates TRPV1 through MAPK and PI3K signaling pathways in a rat model of bone cancer pain [J]. Neuroscience bulletin, 2012, 28(2): 165-172.[29] Zhuang Zhi-ye, Xu Hao-xing, David E Clapham, et al. Phosphatidylinositol 3-kinase activates ERK in primary sensory neurons and mediates inflammatory heat hyperalgesia through TRPV1 sensitization [J]. J Neuroscience, 2004, 24(38): 8300-8309.[30] Renuka Ramachandra, Stephanie Y McGrew, James C Baxter, et al. NaV1.8 channels are expressed in large, as well as small, diameter sensory afferent neurons [J]. Channels, 2013, 7(1): 0-1.[31] Amaya F, Wang H, Costigan M, et al. The voltage-gated sodium channel Nav1. 9 is an effector of peripheral inflammatory pain hypersensitivity [J]. J Neurosci, 2006, 26(50): 12852-12860.[32] Sulayman D Dib-Hajj, Theodore R Cummins, Joel A Black, et al. Sodium channels in normal and pathological pain [J]. Annual Review of Neuroscience, 2010, 33: 325-347.[33] Wu Dai-fei, Dave Chandra, Thomas McMahon, et al. PKCε phosphorylation of the sodium channel NaV1.8 increases channel function and produces mechanical hyperalgesia in mice [J]. J Clinical Investigation, 2012, 122(3): 1306-1315.[34] 肖杭, 戴晓青, 毛霞, 等. 铅抑制大鼠背根神经元外向延迟整流钾通道[J]. 中华预防医学杂志, 2001, 35(2): 108-110.[35] B Hille. Ion channels of excitable membranes [M]. 507, USA, Sinauer Sunderland, MA, 2001[36] Zhu Xiang, Liu Jin-qian, Gao Yong-jing, et al. ATP-sensitive potassium channels alleviate postoperative pain through JNK-dependent MCP-1 expression in spinal cord [J]. Int J Mol Med, 2015, 35(5): 1257-1265.[37] Sang-Min Jeon, Kyung-Min Lee, Hee-Jung Cho. Expression of monocyte chemoattractant protein-1 in rat dorsal root ganglia and spinal cord in experimental models of neuropathic pain [J]. Brain Res, 2009, 1251: 103-111.[38] Wang Chang-hui, Zou Li-jing, Zhang Yi-li, et al. The excitatory effects of the chemokine CCL2 on DRG somata are greater after an injury of the ganglion than after an injury of the spinal or peripheral nerve [J]. Neuroscience Lett, 2010, 475 (1): 48-52.[39] Tatsuro Kohno, Hai-bin Wang, Fumimasa Amaya, et al. Bradykinin enhances AMPA and NMDA receptor activity in spinal cord dorsal horn neurons by activating multiple kinases to produce pain hypersensitivity [J]. J Neuroscience, 2008, 28(17): 4533-4540. [40] Randi? M, He?imovi? H, Ryu P. Substance P modulates glutamate-induced currents in acutely isolated rat spinal dorsal horn neurons[J]. Neuroscience Lett, 1990, 117(1-2): 74-80.[41] Aaron Y Lai, Richard D Swayze, Alaa El-Husseini, et al. Interleukin-1 beta modulates AMPA receptor expression and phosphorylation in hippocampal neurons[J]. J Neuroimmunol, 2006, 175(1-2): 97-106.[42] Chung-Yu Huang, Chen Ying-ling, Allen H Li, et al. Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons[J]. J Neuroinflammation, 2014, 11: 7. [43] Fletcher A White, Sun Ji-hu, Stephen M Waters, et al. Excitatory monocyte chemoattractant protein-1 signaling is up-regulated in sensory neurons after chronic compression of the dorsal root ganglion [J]. Proc Natl Acad Sci of the USA, 2005, 102(39): 14092-14097.[44] Zhou Yan, Tang Hong-mei, Liu Jia-nuo, et al. Chemokine CCL2 modulation of neuronal excitability and synaptic transmission in rat hippocampal slices [J]. J Neurochemistry, 2011, 116(3): 406-414.[45] Gao Yong-jing, Ji Ru-rong. Chemokines, neuronal–glial interactions, and central processing of neuropathic pain [J]. Pharmacology & Therapeutics, 2010, 126(1): 56-68.[46] Cao Jing, Yang Xian, Liu Yan-ni, et al. GABAergic disinhibition induced pain hypersensitivity by upregulating NMDA receptor functions in spinal dorsal horn [J]. Neuropharmacology, 2011, 60(6): 921-929.[47] Arbazia Baamonde, Ana Hidalgo, Luis Menéndez. Involvement of glutamate NMDA and AMPA receptors, glial cells and IL-1β in the spinal hyperalgesia evoked by the chemokine CCL2 in mice [J]. Neuroscience Lett, 2011, 502(3): 178-181.[48] Herman Friedman, Susan Pross, Thomas W Klein. Addictive drugs and their relationship with infectious diseases [J]. FEMS Immunology & Medical Microbiology, 2006, 47(3): 330-342.[49] Avi Nath, Kurt F Hauser, Valerie Wojna, et al. Molecular basis for interactions of HIV and drugs of abuse [J]. JAIDS J Acquired Immune Deficiency Syndromes, 2002, 31(Suppl 2): S62-S69.[50] Toby K Eisenstein, Mary E Hilburger. Opioid modulation of immune responses: effects on phagocyte and lymphoid cell populations [J]. J Neuroimmunology, 1998, 83(1-2): 36-44.[51] Michele A Wetzel, Amber D Steele, Toby K Eisenstein, et al. µ-Opioid induction of monocyte chemoattractant protein-1, RANTES, and IFN-γ-inducible protein-10 expression in human peripheral blood mononuclear cells [J]. J Immunology, 2000, 165(11): 6519-6524.[52] Supriya D Mahajan, Stanley A Schwartz, Ravikumar Aalinkeel, et al. Morphine modulates chemokine gene regulation in normal human astrocytes [J]. Clinical Immunology, 2005, 115(3): 323-332.[53] R Bryan Rock, Hu Shu-xian, Wen S Sheng, et al. Morphine stimulates CCL2 production by human neurons [J]. J Neuroinflammation, 2006, 3:32.[54] Christine Happel, Michele Kutzler, Thomas J Rogers. Opioid-induced chemokine expression requires NF-κB activity: the role of PKCζ [J]. J Leukoc Biol, 2011, 89(2): 301-309.[55] Imre Szabo, Chen Xiao-hong, Xin Lin, et al. Heterologous desensitization of opioid receptors by chemokines inhibits chemotaxis and enhances the perception of pain [J]. Proc Natl Acad Sci USA, 2002, 99(16): 10276-10281.[56] Jon-Kar Zubieta, Smith Y R, Bueller J A, et al. Regional mu opioid receptor regulation of sensory and affective dimensions of pain [J]. Science, 2001, 293(5528): 311-315.[57] Zhang Ning, Thomas J Rogers, Michael Caterina, et al. Proinflammatory chemokines, such as CC chemokine ligand 3, desensitize µ-opioid receptors on dorsal root ganglia neurons [J]. J Immunology, 2004, 173(1): 594-599.[58] Marzia Melcangic, Norman G Bowery. GABA and its receptors in the spinal cord [J]. Trends in pharmacological sciences, 1996, 17 (12): 457-462.[59] T Philip Malan, Heriberto P Mata, Frank Porreca. Spinal GABAA and GABAB receptor pharmacology in a rat model of neuropathic pain [J]. Anesthesiology, 2002, 96(5): 1161-1167.[60] Young S Gwak, Claire E Hulsebosch. GABA and central neuropathic pain following spinal cord injury [J]. Neuropharmacology, 2011, 60(5): 799-808.[61] Romain Daniel Gosselin, Carolina Varela, Banisadr G, et al. Constitutive expression of CCR2 chemokine receptor and inhibition by MCP‐1/CCL2 of GABA‐induced currents in spinal cord neurones [J]. J Neurochemistry, 2005, 95(4): 1023-1034.[62] Hu Ji-hua, Zheng Xiao-yan, Yang Jian-ping, et al. Involvement of spinal monocyte chemoattractant protein-1 (MCP-1) in cancer-induced bone pain in rats [J]. Neuroscience Letters, 2012, 517(1): 60-63. |
[1] | 周欣梅, 朱立平. 四逆散治疗卒中后抑郁的网络药理学研究[J]. 神经药理学报, 2024, 14(5): 19-. |
[2] | 夏蕾, 尤斯涵, 殷宏艳, 郝军荣, 郭春燕. 基于网络药理学方法探讨白芍治疗癫痫的活性成分和作用机制[J]. 神经药理学报, 2024, 14(2): 26-. |
[3] | 陈帆, 任君旭, 张静. 基于网络药理探讨黄芪-柴胡对甲亢的作用机制[J]. 神经药理学报, 2023, 13(5): 6-. |
[4] | 陶瑜晶, 王想福, 谢芋涛, 等. 基于网络药理学分析独活寄生汤治疗椎间盘退变的分子机制[J]. 神经药理学报, 2023, 13(4): 1-. |
[5] | 于美华, 周静, 高士杰, 包金风. Sirtuins在神经退行性疾病中的作用机制[J]. 神经药理学报, 2023, 13(1): 35-. |
[6] | 姚鹏程, 马斌祥, 关永林, 陈国栋, 鄢卫平, 宫玉锁, 郑建鹏, 刘帅. 富血小板血浆治疗腰椎间盘突出症病理性神经痛的作用机制[J]. 神经药理学报, 2023, 13(1): 43-. |
[7] | 范荣珍, 郭宝, 景永帅, 张丹参. 天然药物活性成分对溃疡性结肠炎作用机制研究进展[J]. 神经药理学报, 2022, 12(6): 57-64. |
[8] | 赵朋涛, 闫聚瀚, 闫晓冬, 等. 七叶皂苷钠对肾缺血再灌注的保护作用及机制[J]. 神经药理学报, 2022, 12(5): 17-. |
[9] | 陈帆, 任君旭, 张静. 基于网络药理探讨半夏对肝癌的作用机制[J]. 神经药理学报, 2022, 12(1): 1-10. |
[10] | 张巧巧, 范荣珍, 景永帅, 张丹参. 缺血性脑损伤中的线粒体质量控制[J]. 神经药理学报, 2022, 12(1): 41-47. |
[11] | 陈晓依, 赵靖宇, 陈树春. 代谢性疾病及心脑血管疾病尿外泌体的变化及机制研究进展[J]. 神经药理学报, 2021, 11(6): 60-. |
[12] | 孙玉, 李鹏, 杨鹏飞. 姜黄素抗脑缺血再灌注损伤的药理学研究进展 [J]. 神经药理学报, 2021, 11(4): 38-. |
[13] | 谢佳佳, 孙婷, 张丹参. 线粒体自噬的调控机制及其在脑缺血再灌注损伤中的作用[J]. 神经药理学报, 2021, 11(3): 43-49. |
[14] | 孙婷, 谢佳佳, 张丹参. 线粒体通透性转换孔在脑缺血再灌注损伤中的研究进展 [J]. 神经药理学报, 2021, 11(2): 26-31. |
[15] | 朱晓悫, 张炜. 中药及其有效成分治疗癫痫的作用机制 [J]. 神经药理学报, 2021, 11(2): 45-52. |
阅读次数 | ||||||
全文 |
|
|||||
摘要 |
|
|||||