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Electroacupuncture attenuates spinal nerve ligation-induced microglial activation mediated by p38 mitogen-activated protein kinase
- Chinese Journal of Integrative Medicine Vol. 22, Issue 9, Pages: 704-713(2016)
- Affiliations：
1. Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University,Hangzhou,China
2. Department of Acupuncture and Moxibustion, The Third Affiliated Hospital of Zhejiang Chinese Medical University,Hangzhou,China
3. Department of Acupuncture and Moxibustion, Xixi Hospital of Hangzhou,Hangzhou,China
- Author bio：
- Funds：Supported by National Natural Science Foundation of China (No. 81102643), Zhejiang Provincial Natural Science Foundation (No. Y2091151), State Administration of Traditional Chinese Medicine (Acupuncture) of Key Subjects Construction Funding (No. [2009]30), and Research Fund of Zhejiang Provincial First-Foremost Key Subject—Acupuncture and Moxibustion (No. [2008]255)
DOI：10.1007/s11655-015-2045-1
CLC：Published：2016，
Published Online：6 April 2015，
Scan for full text
Liang, Y., Du, Jy., Qiu, Yj. et al. Electroacupuncture attenuates spinal nerve ligation-induced microglial activation mediated by p38 mitogen-activated protein kinase., Chin. J. Integr. Med. 22, 704–713 (2016). https://doi.org/10.1007/s11655-015-2045-1
Yi Liang, Jun-ying Du, Yu-jie Qiu, et al. Electroacupuncture attenuates spinal nerve ligation-induced microglial activation mediated by p38 mitogen-activated protein kinase. [J]. Chinese Journal of Integrative Medicine 22(9):704-713(2016)
Liang, Y., Du, Jy., Qiu, Yj. et al. Electroacupuncture attenuates spinal nerve ligation-induced microglial activation mediated by p38 mitogen-activated protein kinase., Chin. J. Integr. Med. 22, 704–713 (2016). https://doi.org/10.1007/s11655-015-2045-1 DOI：
Yi Liang, Jun-ying Du, Yu-jie Qiu, et al. Electroacupuncture attenuates spinal nerve ligation-induced microglial activation mediated by p38 mitogen-activated protein kinase. [J]. Chinese Journal of Integrative Medicine 22(9):704-713(2016) DOI： 10.1007/s11655-015-2045-1.
摘要
To investigate whether analgesic effect of electroacupuncture (EA) is affected by p38 mitogen-activated protein kinase (p38 MAPK) on microglia. There were two experiments. The experiment 1: 40 male Sprague-Dawley (SD) rats were randomly divided into the normal
surgery
EA and sham EA groups
and the L5 spinal nerve ligation (SNL) on the right side was used to establish neuropathic pain model. EA was applied to bilateral Zusanli (ST36) and Kunlun (BL60) at 24
48 and 72 h after SNL for 30 min
once per day. The paw withdrawal thresholds (PWTs) were measured before surgery (as base) and at 24
25
49 and 73 h after surgery. Phospho-p38 MAPK (p-p38 MAPK)
oxycocin-42 (OX-42
marker of microglia)
and glial fibrillary acidic protein (GFAP
marker of astrocyte) in bilateral spinal cord dorsal horn (SCDH) were detected by immunofluorescence
respectively. The experiment 2: 40 male SD rats were cannulated for SNL-induced neuropathic pain
and then were randomly divided into the dimethyl sulfoxide (DMSO)
EA plus DMSO
4-(4-fluorophenyl)-2-(4-methylsulfonylpheny)-5-(4-pyridyl)-1H-imidazole (SB203580) and EA plus SB203580 groups. SB203580 (30 nmol/L) was administered 5 min prior to EA treatment. The PWTs and OX-42 in bilateral SCDH were measured as mentioned above. SNL-induced neuropathic pain reduced PWTs and increased the expression of p-p38 MAPK and OX-42 in bilateral lumbar SCDH of rats (P<0.01). Spinal p-p38 MAPK was only co-localized with OX-42 in our study. EA treatment significantly alleviated SNL-mediated mechanical hyperalgesia
and suppressed the expression of p-p38 MAPK and OX-42 in lumbar SCDH (P<0.05 or P<0.01). Intrathecal injection of low dose SB203580 had no influence on PWTs (P>0.05)
but significantly inhibited the expression of OX-42 positive cells in bilateral SCDH (P<0.01 or P<0.05). EA plus SB203580 synergistically increased PWTs
and reduced the expression of bilateral spinal OX-42 (P<0.01 or P<0.05). The central mechanism of EA-induced anti-hyperalgesia may be partially associated with the reduced expression of p-p38 MAPK
and subsequently reducing the activation of OX-42 in neuropathic pain. Therefore
EA may be a new complementary and alternative therapy for neuropathic pain.
Abstract
To investigate whether analgesic effect of electroacupuncture (EA) is affected by p38 mitogen-activated protein kinase (p38 MAPK) on microglia. There were two experiments. The experiment 1: 40 male Sprague-Dawley (SD) rats were randomly divided into the normal
surgery
EA and sham EA groups
and the L5 spinal nerve ligation (SNL) on the right side was used to establish neuropathic pain model. EA was applied to bilateral Zusanli (ST36) and Kunlun (BL60) at 24
48 and 72 h after SNL for 30 min
once per day. The paw withdrawal thresholds (PWTs) were measured before surgery (as base) and at 24
25
49 and 73 h after surgery. Phospho-p38 MAPK (p-p38 MAPK)
oxycocin-42 (OX-42
marker of microglia)
and glial fibrillary acidic protein (GFAP
marker of astrocyte) in bilateral spinal cord dorsal horn (SCDH) were detected by immunofluorescence
respectively. The experiment 2: 40 male SD rats were cannulated for SNL-induced neuropathic pain
and then were randomly divided into the dimethyl sulfoxide (DMSO)
EA plus DMSO
4-(4-fluorophenyl)-2-(4-methylsulfonylpheny)-5-(4-pyridyl)-1H-imidazole (SB203580) and EA plus SB203580 groups. SB203580 (30 nmol/L) was administered 5 min prior to EA treatment. The PWTs and OX-42 in bilateral SCDH were measured as mentioned above. SNL-induced neuropathic pain reduced PWTs and increased the expression of p-p38 MAPK and OX-42 in bilateral lumbar SCDH of rats (P<0.01). Spinal p-p38 MAPK was only co-localized with OX-42 in our study. EA treatment significantly alleviated SNL-mediated mechanical hyperalgesia
and suppressed the expression of p-p38 MAPK and OX-42 in lumbar SCDH (P<0.05 or P<0.01). Intrathecal injection of low dose SB203580 had no influence on PWTs (P>0.05)
but significantly inhibited the expression of OX-42 positive cells in bilateral SCDH (P<0.01 or P<0.05). EA plus SB203580 synergistically increased PWTs
and reduced the expression of bilateral spinal OX-42 (P<0.01 or P<0.05). The central mechanism of EA-induced anti-hyperalgesia may be partially associated with the reduced expression of p-p38 MAPK
and subsequently reducing the activation of OX-42 in neuropathic pain. Therefore
EA may be a new complementary and alternative therapy for neuropathic pain.
关键词
electroacupunctureneuropathic painmicrogliap38 mitogen-activated protein kinaseoxycocin-42
Keywords
electroacupunctureneuropathic painmicrogliap38 mitogen-activated protein kinaseoxycocin-42
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