Skip NavigationSkip to Content
Return Return to Search Results

The antishock effect of anisodamine requires the upregulation of alpha 7 nicotine acetylcholine receptors by IL-10

  1. Author:
    Li, Q.
    Lei, H.
    Liu, A. J.
    Yang, Y. L.
    Su, D. F.
    Liu, X.

  2. Author Address

    [Li, Q; Lei, H; Liu, AJ; Su, DF; Liu, X] Mil Med Coll 2, Sch Pharm, Dept Pharmacol, Shanghai 200433, Peoples R China. [Yang, YL] NCI, Canc & Dev Biol Lab, NIH, Frederick, MD 21702 USA.;Su, DF (reprint author), Mil Med Coll 2, Sch Pharm, Dept Pharmacol, 325 Guo He Rd, Shanghai 200433, Peoples R China;dfsu2008@gmail.com lxflying@yahoo.com.cn
    1. Year: 2011
    2. Date: Sep
  2. Journal: Life Sciences
    1. 89
    2. 11-12
    3. Pages: 395-401
  4. Type of Article: Article
  5. ISSN: 0024-3205
  1. Abstract:

    Aims: Although anisodamine, a muscarinic acetylcholine receptor antagonist, has been used in China for treating various shocks for many years, the mechanisms are not well understood. Our previous studies have demonstrated anisodamine exerts its cholinergic anti-inflammatory action through indirectly activating alpha 7 nicotinic acetylcholine receptors (alpha 7 nAChR). Because IL-10 is a critical anti-inflammatory factor, we investigated its potential role in the antishock action of anisodamine. Main methods: C57BL/6 and IL-10-/- mice were intraperitoneally administered LPS and/or anisodamine, and the 24 h survival rate, cytokine production and alpha 7 nAChR expression were examined. In addition, RAW264.7 cells were stimulated with LPS, anisodamine and/or IL-10, and cytokine production and alpha 7 nAChR expression were investigated. Key findings: Anisodamine dose-dependently increased the 24 h survival rate of C57BL/6 mice treated with LPS. The antishock role of anisodamine was significantly attenuated in IL-10-/- mice. Anisodamine significantly decreased TNF-alpha and IL-1 beta production in LPS-treated RAW264.7 cells and C57BL/6 mice. However, it did not increase the level of IL-10 in the same experiments. In RAW264.7 cells, IL-10 treatment increased alpha 7 nAChR expression, which was further augmented in the presence of anisodamine. Spleens from IL-10-/- mice expressed significantly lower alpha 7 nAChRs levels compared to IL-10+/+ mice. Although anisodamine markedly increased the expression of alpha 7 nAChRs in spleens from LPS-treated IL-10+/+ mice, it only induced a marginal increase of the receptor in spleens from LPS-treated IL-10-/- mice. Significance: These findings demonstrate that IL-10 plays an important role in the antishock action of anisodamine. It acts through upregulating alpha 7nAChR synergistically with anisodamine. Crown Copyright (C) 2011 Published by Elsevier Inc. All rights reserved.

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1016/j.lfs.2011.07.008
  3. View record in Web of Science®
  4. WOS: 000294397800007

Library Notes

  1. Fiscal Year: FY2011-2012
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel