Hu Man-Li, Zhou Fei-Yan, Liu Jing-Jing, Ding Yi, Zhong Ju-Ming, Ding Ming-Xing
College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.
College of Veterinary Medicine, Auburn University, 212 Greene Hall, Auburn, AL 36849-5518, USA.
Evid Based Complement Alternat Med. 2017;2017:7531060. doi: 10.1155/2017/7531060. Epub 2017 Nov 22.
The mitogen-activated protein kinases (MAPKs), especially p38MAPK, play a pivotal role in chronic pain. Electroacupuncture (EA) relieves inflammatory pain underlying the descending pathway, that is, the periaqueductal gray (PAG), the rostral ventromedial medulla (RVM), and the spinal cord dorsal horn (SCDH). However, whether EA antagonizes inflammatory pain through regulation of p38MAPK in this descending facilitatory pathway is unclear. Complete Freund's adjuvant (CFA) was injected into the hind paw of rats to establish inflammatory pain model. EA was administrated for 30 min at Zusanli and Kunlun acupoints at 0.5, 24.5, 48.5, and 72.5 h, respectively. The paw withdrawal threshold (PWT), paw edema, and Phosphor-p38MAPK-Immunoreactivity (p-p38MAPK-IR) cells were measured before (0 h) and at 1, 3, 5, 7, 25, and 73 h after CFA or saline injection. EA increased PWT at 1, 3, 25, and 73 h and inhibited paw edema at 25 and 73 h after CFA injection. Moreover, the increasing number of p-p38MAPK-IR cells which was induced by CFA was suppressed by EA stimulation in PAG and RVM at 3 and 5 h and in SCDH at 5, 7, 25, and 73 h. These results suggest that EA suppresses inflammation-induced hyperalgesia probably through inhibiting p38MAPK activation in the descending facilitatory pathway.
丝裂原活化蛋白激酶（MAPKs），尤其是p38丝裂原活化蛋白激酶（p38MAPK），在慢性疼痛中起关键作用。电针（EA）可缓解下行通路（即中脑导水管周围灰质（PAG）、延髓头端腹内侧网状结构（RVM）和脊髓背角（SCDH））所介导的炎性疼痛。然而，EA是否通过调节该下行易化通路中的p38MAPK来拮抗炎性疼痛尚不清楚。将完全弗氏佐剂（CFA）注射到大鼠后爪以建立炎性疼痛模型。分别在0.5、24.5、48.5和72.5小时于足三里和昆仑穴给予EA治疗30分钟。在注射CFA或生理盐水前（0小时）以及注射后1、3、5、7、25和73小时测量爪缩足阈值（PWT）、爪肿胀程度以及磷酸化p38MAPK免疫反应性（p-p38MAPK-IR）细胞数量。EA可使CFA注射后1、3、2以及73小时的PWT升高，并抑制25和73小时的爪肿胀。此外，CFA诱导的p-p38MAPK-IR细胞数量增加在3和5小时时被PAG和RVM中的EA刺激所抑制，在5、7、25和73小时时被SCDH中的EA刺激所抑制。这些结果表明，EA可能通过抑制下行易化通路中p38MAPK的激活来抑制炎症诱导的痛觉过敏。
