Inhibition of spinal interlukin-33/ST2 signaling and downstream ERK and JNK pathways in electroacupuncture analgesia in formalin mice

29Citations
Citations of this article
37Readers
Mendeley users who have this article in their library.

Abstract

Although acupuncture is widely used to manage pain, it remains highly controversial, largely due to the lack of a clear mechanism for its benefits. Here, we investigated the role of IL-33, a novel interleukin (IL)-1 family member, and its receptor ST2 in the analgesic effects of electroacupuncture (EA) on formalin-induced inflammatory pain. The results showed that 1) EA stimulation of ipsilateral Zusanli (ST 36) and Yanglingquan (GB 34) acupoints for 30 min remarkably suppressed the two phases of formalin-induced spontaneous pain; 2) subcutaneous or intrathecal administration of recombinant IL-33 (rIL-33) significantly inhibited the analgesic effect of EA, whereas the ST2 antibody potentiated EA analgesia in formalin mice; 3) EA treatment decreased the up-regulation of IL-33 and ST2 protein following formalin injection; and 4) the suppression of the formalin-induced expression of spinal phosphorylated ERK and JNK induced by EA treatment was significantly attenuated following subcutaneous rIL-33 delivery, and was further decreased by the ST2 antibody. These data suggest that EA alleviates formalin-induced inflammatory pain, at least partially, by inhibiting of spinal IL-33/ST2 signaling and the downstream ERK and JNK pathways.

Cite

CITATION STYLE

APA

Han, P., Liu, S., Zhang, M., Zhao, J., Wang, Y., Wu, G., & Mi, W. M. (2015). Inhibition of spinal interlukin-33/ST2 signaling and downstream ERK and JNK pathways in electroacupuncture analgesia in formalin mice. PLoS ONE, 10(6). https://doi.org/10.1371/journal.pone.0129576

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free