Orginal Article

Effect of Electroacupuncture at Baihui and Siguan on Expression of Tax1-binding Protein 1 in Cerebral Cortex in Focal Cerebral Ischemia-Reperfusion Rats

  • MA Hong-mei ,
  • JIANG Jin ,
  • ZHAN Jian ,
  • LI Qiong-li ,
  • ZHANG Ying ,
  • QIN Wen-yi ,
  • LUO Yong
Expand
  • 1.a. Department of Neurology, b. Department of Integrated Chinese and Western Medicine, the First Affiliated Hospital of Chonqing Medical University, Chongqing 400016, China;
    2.Chongqing Key laboratory of Neurology, Chongqing 400016, China

Received date: 2017-07-18

  Revised date: 2017-11-08

  Online published: 2017-12-28

Abstract

Objective To observe the effect of electroacupuncture (EA) at Baihui (GV20) and Siguan (Hegu/LI4 and Taichong/LR3) of affected side on expression of Tax1-binding protein 1 (TAX1BP1) in cerebral cortex in focal cerebral ischemia-reperfusion rats, so as to investigate its protective mechanism in inhibiting nuclear factor kappa B (NF-κB) signaling pathway and promoting neurobehavioral recovery. Methods A total of 105 Sprague-Dawley rats were randomly assigned into sham group, model group and EA group. Each group was randomly assigned into reperfusion six hours, twelve hours, 24 hours, 48 hours, 72 hours groups after two hours of ischemia. The model was established by right middle cerebral artery occlusion and reperfusion. EA group received electroacupuncture at Baihui and left Siguan (Hegu and Taichong) acupoints. Neurobehavioral evaluation, TAX1BP1 protein expression, TAX1BP1 positive cell count, zink finger protein A20 expression, and nuclear NF-κB p65 protein expression were tested in each group. Results There was no neurological deficit in the sham group. Compared with the model group, the neurological scores at 48 hours, 72 hours after reperfusion decreased in EA group (P<0.05). Compared with the control group, the TAX1BP1 expression at twelve hours, 24 hours and 48 hours after reperfusion increased in the model group (P<0.05), and further increased at twelve hours, 24 hours, 48 hours and 72 hours after reperfusion in EA group (P<0.05), and peaked at 24 hours after reperfusion. Compared with the sham group, the expression of A20 and NF-κB p65, and the number of TAX1BP1 positive cells increased in the model group (P<0.05), and the expression of A20 and the number of TAX1BP1 positive cells further increased, (P<0.05) and the expression of NF-κB p65 decreased in EA group (P<0.05) at 24 hours after reperfusion. Immunofluorescence labeling indicated that TAX1BP1 protein primarily expressed in the cytoplasm, TAX1BP1 protein and A20 protein co-expressed in the cytoplasm. Immunohistochemistry showed indicated that NF-κB p65 mainly expressed in the nucleus in the model groupr, and mainly expressed in the cytoplasm in the EA group. Conclusion Electroacupuncture could significantly inhibit neuronal NF-κB signaling pathway and promote neurobehavioral recovery in focal cerebral ischemia-reperfusion, which may related with up-regulating TAX1BP1 protein expression.

Cite this article

MA Hong-mei , JIANG Jin , ZHAN Jian , LI Qiong-li , ZHANG Ying , QIN Wen-yi , LUO Yong . Effect of Electroacupuncture at Baihui and Siguan on Expression of Tax1-binding Protein 1 in Cerebral Cortex in Focal Cerebral Ischemia-Reperfusion Rats[J]. Chinese Journal of Rehabilitation Theory and Practice, 2017 , 23(12) : 1372 -1379 . DOI: 10.3969/j.issn.1006-9771.2017.12.002

References

[1] 贾建平,陈生弟. 神经病学[M]. 7版. 北京:人民卫生出版社, 2013: 170.
[2] Abou-Chebl A. Management of acute ischemic stroke [J]. Curr Cardiol Rep, 2013, 15(4): 348.
[3] Liu L, Wang D, Wong KS, et al. Stroke and stroke care in China: huge burden, significant workload, and a national priority [J]. Stroke, 2011, 42(12): 3651-3654.
[4] Petrovic-Djergovic D, Goonewardena SN, Pinsky DJ. Inflammatory disequilibrium in stroke [J]. Circ Res, 2016, 119(1): 142-158.
[5] Shih RH, Wang CY, Yang CM. NF-kappaB signaling pathways in neurological inflammation: a mini review [J]. Front Mol Neurosci, 2015, 8: 77.
[6] Chin KT, Chun AC, Ching YP, et al. Human T-cell leukemia virus oncoprotein tax represses nuclear receptor-dependent transcription by targeting coactivator TAX1BP1 [J]. Cancer Res, 2007, 67(3): 1072-1081.
[7] Shembade N, Harhaj NS, Liebl DJ, et al. Essential role for TAX1BP1 in the termination of TNF-alpha-, IL-1- and LPS-mediated NF-kappaB and JNK signaling [J]. EMBO J, 2007, 26(17): 3910-3922.
[8] Lim SM, Yoo J, Lee E, et al. Acupuncture for spasticity after stroke: a systematic review and meta-analysis of randomized controlled trials [J]. Evid Based Complement Alternat Med, 2015, 2015: 870398.
[9] 秦文熠,罗勇,余超. 电针对局灶性脑缺血再灌注大鼠海马内白介素-1&#x#x003b2;及转录核因子&#x#x003ba;B抑制蛋白激酶的影响[J]. 针刺研究, 2013, 38(4): 271-276.
[10] Qin WY, Luo Y, Chen L, et al. Electroacupuncture could regulate the NF-&#x#x003ba;B signaling pathway to ameliorate the inflammatory injury in focal cerebral ischemia/reperfusion model rats [J]. Evid Based Complement Alternat Med, 2013, 2013: 924541.
[11] Zhan J, Qin W, Zhang Y, et al. Upregulation of neuronal zinc finger protein A20 expression is required for electroacupuncture to attenuate the cerebral inflammatory injury mediated by the nuclear factor-kB signaling pathway in cerebral ischemia/reperfusion rats [J]. J Neuroinflammation, 2016, 13(1): 258.
[12] 华兴邦,周浩良. 大鼠穴位图谱的研制[J]. 实验动物与动物实验, 1991(1): 1-5.
[13] Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats [J]. Stroke, 1989, 20(1): 84-91.
[14] Writing Group Members. Mozaffarian D, Benjamin EJ, Go AS, et al. Executive summary: heart disease and stroke statistics&#x#x02013;2016 update: a report from the American Heart Association [J]. Circulation, 2016, 133(4): 447-454.
[15] Vidale S, Consoli A, Arnaboldi M, et al. Postischemic inflammation in acute stroke [J]. J Clin Neurol, 2017, 13(1): 1-9.
[16] Carden DL, Granger DN. Pathophysiology of ischaemia-reperfusion injury [J]. J Pathol, 2000, 190(3): 255-266.
[17] Mezzasoma L, Antognelli C, Talesa VN. A novel role for brain natriuretic peptide: Inhibition of IL-1&#x#x003b2; secretion via downregulation of NF-&#x#x003ba;B/Erk 1/2 and NALP3/ASC/caspase-1 activation in human THP-1 monocyte [J]. Mediators Inflamm, 2017, 2017: 5858315.
[18] Verma IM, Stevenson JK, Schwarz EM, et al. Rel/NF-kappa B/I kappa B family: intimate tales of association and dissociation [J]. Genes Dev, 1995, 9(22): 2723-2735.
[19] Baeuerle PA, Baltimore D. NF-kappa B: ten years after [J]. Cell, 1996, 87(1): 13-20.
[20] Miyamoto S. Nuclear initiated NF-&#x#x003ba;B signaling: NEMO and ATM take center stage [J]. Cell Res, 2011, 21(1): 116-130.
[21] Lan L, Tao J, Chen A, et al. Electroacupuncture exerts anti-inflammatory effects in cerebral ischemia-reperfusion injured rats via suppression of the TLR4/NF-&#x#x003ba;B pathway [J]. Int J Mol Med, 2013, 31(1): 75-80.
[22] Liu W, Wang X, Zheng Y, et al. Electroacupuncture inhibits inflammatory injury by targeting the miR-9-mediated NF-&#x#x003ba;B signaling pathway following ischemic stroke [J]. Mol Med Rep, 2016, 13(2): 1618-1626.
[23] Boxus M, Twizere JC, Legros S, et al. The HTLV-1 Tax interactome [J]. Retrovirology, 2008, 5: 76.
[24] Iha H, Kasai T, Kibler KV, et al. Pleiotropic effects of HTLV type 1 Tax protein on cellular metabolism: mitotic checkpoint abrogation and NF-kappaB activation [J]. AIDS Res Hum Retroviruses, 2000, 16(16): 1633-1638.
[25] Journo C, Filipe J, About F, et al. NRP/Optineurin Cooperates with TAX1BP1 to potentiate the activation of NF-kappaB by human T-lymphotropic virus type 1 tax protein [J]. PLoS Pathog, 2009, 5(7): e1000521.
[26] Chen ZJ. Ubiquitination in signaling to and activation of IKK [J]. Immunol Rev, 2012, 246(1): 95-106.
[27] Morriswood B, Ryzhakov G, Puri C, et al. T6BP and NDP52 are myosin VI binding partners with potential roles in cytokine signalling and cell adhesion [J]. J Cell Sci, 2007, 120(Pt 15): 2574-2585.
[28] Bannon A, Zhang SD, Schock BC, et al. Cystic fibrosis from laboratory to bedside: the role of A20 in NF-&#x#x003ba;B-mediated inflammation [J]. Med Princ Pract, 2015, 24(4): 301-310.
[29] Wertz IE, O'Rourke KM, Zhou H, et al. De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-kappaB signaling [J]. Nature, 2004, 430(7000): 694-699.
[30] Skaug B, Chen J, Du F, et al. Direct, noncatalytic mechanism of IKK inhibition by A20 [J]. Mol Cell, 2011, 44(4): 559-571.
[31] Iha H, Peloponese JM, Verstrepen L, et al. Inflammatory cardiac valvulitis in TAX1BP1-deficient mice through selective NF-kappaB activation [J]. EMBO J, 2008, 27(4): 629-641.
Outlines

/