蜂毒针刺减轻脊髓损伤压迫模型中调节小胶质细胞/巨噬细胞表型极化的神经炎症

Raquel De Souza, Júlia Miccolis Azevedo Lopes, L. R. Monteiro, R. A. Barbosa, Gabriela Hollmann, S. Allodi, L. Reis, M. Medeiros
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引用次数: 0

摘要

目的:本研究旨在探讨针刺(蜂毒刺激穴位)ST36和GV3穴是否通过调节M1和M2表型极化来促进神经保护和减轻神经炎症。方法:用蜂毒(BV) (0.08 mg/kg)注射于Wistar大鼠ST36和GV3穴[BV (ST36 + GV3)-脊髓损伤(SCI)]或BV注射于非穴位[BV (NP)-SCI]或脊髓损伤后不治疗(CTL-SCI)]。real - time PCR检测大鼠脊髓iNOS、Arg-1、TGF-β mRNA表达及IBA-1水平;bcl - 2;western blotting检测NeuN - CNPase。运动表现采用Basso, Beattie, and Bresnahan (BBB)测试和网格行走测试。结果:针刺治疗能够(1)改善运动能力;(2)降低炎症标志物(Cox-2水平)和小胶质细胞和巨噬细胞的活化;(3)减少M1表型标记物(iNOS)的极化,增加M2 (Arg-1和TGF-β)表型标记物;(4)通过减少神经元和少突胶质细胞的死亡来促进神经保护;(5)增加抗凋亡因子BCL-2的表达。结论:针刺治疗可促进脊髓损伤模型后的运动恢复和神经保护。此外,它通过减少M1极化和增加M2来减轻神经炎症
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Bee venom acupuncture reduces neuroinflammation modulating microglia/macrophage phenotype polarization in spinal cord injury compression model
Aim: The present study aimed to examine whether apipuncture (stimulation of acupuncture points with bee venom) at ST36 and GV3 acupoints promotes neuroprotection and reduces neuroinflammation by modulating M1 and M2 phenotype polarization. Methods: Wistar rats were treated with bee venom (BV) (0.08 mg/kg) injection at acupoints ST36 and GV3 [BV (ST36 + GV3)-spinal cord injury (SCI)] or BV injection at non-acupoints [BV (NP)-SCI] or no treatment (CTL-SCI) after SCI by compression. The spinal cord mRNA expression of iNOS, Arg-1 and TGF-β was measured by real time PCR and the levels of IBA-1; BCL-2; NeuN e CNPase was measured by western blotting. Locomotor performance was measured by Basso, Beattie, and Bresnahan (BBB) and grid-walking tests. Results: Apipuncture treatment was able to (1) ameliorate locomotor performance; (2) reduce inflammatory markers (Cox-2 levels) and activation of microglia and macrophages; (3) reduce the polarization of the M1 phenotype marker (iNOS) and increase M2 (Arg-1 and TGF-β) phenotypic markers; (4) promote neuroprotection by reducing the death of neurons and oligodendrocytes; and (5) increase the expression of the anti-apoptotic factor BCL-2. Conclusion: Apipuncture treatment induces locomotor recovery and neuroprotection after the compression model of spinal cord injury. Further, it reduces neuroinflammation by decreasing M1 polarization and increasing M2
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