Format

Send to

Choose Destination
See comment in PubMed Commons below
Environ Toxicol Pharmacol. 2013 Mar;35(2):335-46. doi: 10.1016/j.etap.2013.01.004. Epub 2013 Jan 14.

Acanthopanax senticosus exerts neuroprotective effects through HO-1 signaling in hippocampal and microglial cells.

Author information

1
Department of Microbiology, Pusan National University, Busan 609-735, Republic of Korea.

Abstract

Extracts of Acanthopanax senticosus, a traditional herb commonly found in Northeastern Asia, are used for treating neurodegenerative disorders such as ischemia and depression. However, the mechanisms of its neuroinflammatory and cytoprotective effects have not been investigated. We examined the mechanism of A. senticosus activity in anti-neuroinflammatory and neuroprotective processes. HO-1 is an inducible enzyme present in most cell lines. ASE increased HO-1 expression, which reduced LPS-induced nitric oxide/ROS production in BV2 cells. Moreover, the induction of HO-1 expression protected cells against glutamate-induced neuronal cell death. Activation of the p38-CREB pathway and translocation of Nrf2 are strongly involved in ASE-induced HO-1 expression. Our results showed that ASE-induced HO-1 expression through the p38-CREB pathway plays an important role in the generation of anti-neuroinflammatory and neuroprotective responses. ASE also increases the translocation of Nrf2 to regulate HO-1 expression. Furthermore, our results indicate that ASE serves as a potential therapeutic agent for neuronal disorders.

PMID:
23395777
DOI:
10.1016/j.etap.2013.01.004
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center