|
|
The effect of botulinum toxin A on the expression of inflammatory neurotransmitters in mice with postherpetic neuralgia |
LI Guosong, TANG Yanghua, XU Canda, SHEN Zhi’en, LIN Chengying |
Department of Pain Treatment, Xiaoshan TCM Hospital, Hangzhou 311200, China |
|
Cite this article: |
LI Guosong,TANG Yanghua,XU Canda, et al. The effect of botulinum toxin A on the expression of inflammatory neurotransmitters in mice with postherpetic neuralgia[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2020, 50(1): 51-55.
|
|
Abstract Objective: To explore the mechanism of botulinum toxin A (BTX-A) on postherpetic neuralgia (PHN) by observing its effect on the expression of inflammatory neurotransmitter in mice with PNH. Methods: Thirty-six male C57 mice with PHN were randomly divided as group A, B and C, with 12 mice in each group. Herpes site in group A was injected with 0.9% saline, with BTX-A (2 U/kg) in group B, while BTX-A (2 U/kg) was injected into dorsal root ganglion (DRG) of the fifth lumber spine in group C. All mice were sacrificed after 7 d of continuous intervention, and DRG and corresponding segments of spinal cord were isolated from mice. The mRNA expression levels of TNF-α, IL-1β and neurokinin A in DRG and spinal cord was detected by RT-qPCR and ELISA. The expression of Na1.3 and Na1.8 channels in DRG and spinal cord was detected by Western blot. Results: RT-qPCR results showed that the mRNA expression levels of inflammatory neurotransmitters on TNF-α, IL-1β and neurokinin A in group B and group C were significantly lower than those in group A (P<0.05), but there was no significant difference between group B and group C. The results of ELISA showed that the protein contents of TNF-α, IL-1β and neurokinin A in group B and group C were significantly lower than those in group A (P<0.05), but there was no significant difference between group B and group C. Western blot results showed that the expression of Na1.3 and Na1.8 channel proteins in group B and group C decreased significantly compared with group A (P<0.05), but there was no statistical difference between the two groups. Conclusion: BTX-A can effectively inhibit PHN, and its mechanism may be by reducing the expression of Na1.3 and Na1.8 channel proteins and thus inhibiting the expression of inflammatory neurotransmitters TNF-α, IL-1β and neurokinin A.
|
Received: 15 June 2019
|
|
|
|
|
[1] KE M, YINGHUI F, YI J, et al. Efficacy of pulsed radiofrequency in the treatment of thoracic postherpetic neuralgia from the angulus costae: a randomized, double-blinded, controlled trial[J]. Pain Physician, 2013, 16(1): 15-25.
[2] FORBES H J, BHASKARAN K, THOMAS S L, et al. Quantification of risk factors for postherpetic neuralgia in herpes zoster patients: A cohort study[J]. Neurology, 2016, 87(1): 94-102.
[3] ALICINO C, TRUCCHI C, PAGANINO C, et al. Incidence of herpes zoster and post-herpetic neuralgia in Italy: Results from a 3-years population-based study[J]. Hum Vaccin Immunother, 2017, 13(2): 399-404.
[4] 薛锐灵, 颜凤华. A型肉毒毒素对疱疹后神经痛患者疗效及安全性分析[J]. 中南医学科学杂志, 2017, 45(6): 619-621.
[5] RAMACHANDRAN R, YAKSH T L. Therapeutic use of botulinum toxin in migraine:mechanisms of action[J]. Br J Pharmacol, 2014, 171(18): 4177-4192.
[6] 利雪阳, 王云, 郭瑞娟, 等. A型肉毒素预先给药对切口痛大鼠脊髓背角神经激肽-1受体内化的影响[J]. 中华麻醉学杂志, 2016, 36(11): 1356-1360.
[7] LI D, XIAO L. Combining botulinum toxin (A) injection with peripheral nerve stimulation in a patient for intractable ophthalmic postherpetic neuralgia[J]. Neuromodulation, 2015, 18(8): 769-771.
[8] APALLA Z, SOTIRIOU E, LALLAS A, et al. Botulinum toxin A in postherpetic neuralgia: a parallel, randomized, double-blind, single-dose, placebo-controlled trial[J]. Clin J Pain, 2013, 29(10): 857-864.
[9] 杨帆, 李雅琴, 刘孝兵, 等. 肉毒毒素治疗带状疱疹后神经痛的疗效观察及其对血浆β-内啡肽的影响[J]. 河北医学, 2014, 20(6): 937-940.
[10] 历洋, 董道松, 于雪, 等. 牛痘疫苗接种家兔炎症皮肤提取物多途径给药治疗带状疱疹性神经痛的临床观察[J]. 中国疼痛医学杂志, 2017, 23(2): 156-158
[11] 许洁, 许纲. 带状疱疹后遗神经痛与Th1/Th2细胞因子及血清炎性因子相关性探讨[J]. 标记免疫分析与临床, 2017, 24(6): 666-669.
[12] GARRY E M, DELANEY A, ANDERSON H A, et al. Varicella zoster virus induces neuropathic changes in rat dorsal root ganglia and behavioral reflex sensitisation that is attenuated by gabapentin or sodium channel blocking drugs[J]. Pain, 2005, 118(12): 97-111. |
|
|
|