Format

Send to

Choose Destination
See comment in PubMed Commons below
Mediators Inflamm. 2014;2014:493480. doi: 10.1155/2014/493480. Epub 2014 Jul 24.

Auricular electroacupuncture reduced inflammation-related epilepsy accompanied by altered TRPA1, pPKCα, pPKCε, and pERk1/2 signaling pathways in kainic acid-treated rats.

Author information

1
Graduate Institute of Acupuncture Science, College of Chinese Medicine, China Medical University, Taichung 40402, Taiwan ; Research Center for Chinese Medicine & Acupuncture, China Medical University, Taichung 40402, Taiwan.
2
Research Center for Chinese Medicine & Acupuncture, China Medical University, Taichung 40402, Taiwan ; Graduate Institute of Integrative Medicine, College of Chinese Medicine, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan ; Department of Chinese Medicine, China Medical University Hospital, Taichung 40402, Taiwan.

Abstract

BACKGROUND:

Inflammation is often considered to play a crucial role in epilepsy by affecting iron status and metabolism. In this study, we investigated the curative effect of auricular acupuncture and somatic acupuncture on kainic acid- (KA-) induced epilepsy in rats.

METHODS:

We established an epileptic seizure model in rats by KA (12 mg, ip). The 2 Hz electroacupuncture (EA) was applied at auricular and applied at Zusanli and Shangjuxu (ST36-ST37) acupoints for 20 min for 3 days/week for 6 weeks beginning on the day following the KA injection.

RESULTS:

The electrophysiological results indicated that neuron overexcitation occurred in the KA-treated rats. This phenomenon could be reversed among either the auricular EA or ST36-ST37 EA treatment, but not in the sham-control rats. The Western blot results revealed that TRPA1, but not TRPV4, was upregulated by injecting KA and could be attenuated by administering auricular or ST36-ST37 EA, but not in the sham group. In addition, potentiation of TRPA1 was accompanied by increased PKCα and reduced PKCε. Furthermore, pERK1/2, which is indicated in inflammation, was also increased by KA. Furthermore, the aforementioned mechanisms could be reversed by administering auricular EA and could be partially reversed by ST36-ST37 EA.

CONCLUSIONS:

These results indicate a novel mechanism for treating inflammation-associated epilepsy and can be translated into clinical therapy.

PMID:
25147437
PMCID:
PMC4131505
DOI:
10.1155/2014/493480
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Hindawi Publishing Corporation Icon for PubMed Central
    Loading ...
    Support Center