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BJA Advance Access published online on November 20, 2009
British Journal of Anaesthesia, doi:10.1093/bja/aep336
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© The Author [2009]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournal.org

L-type calcium channels are involved in mediating the anti-inflammatory effects of magnesium sulphate

C. Y. Lin1, P. S. Tsai2, Y. C. Hung1 and C. J. Huang3,4,5,*

1 Department of Anaesthesiology, Mackay Memorial Hospital, Taipei, Taiwan, Republic of China.
2 Graduate Institute of Nursing and
3 Department of Pharmacology, Taipei Medical University, Taipei, Taiwan, Republic of China.
4 Department of Anaesthesiology, Buddhist Tzu Chi General Hospital, Taipei Branch, Taipei, Taiwan, Republic of China.
5 School of Medicine, Tzu Chi University, Hualien, Taiwan, Republic of China

* Corresponding author. E-mail: huangcj1112{at}gmail.com

Background: Magnesium sulphate (MgSO4) has potent anti-inflammatory capacity. It is a natural calcium antagonist and a potent L-type calcium channel inhibitor. We sought to elucidate the possible role of calcium, the L-type calcium channels, or both in mediating the anti-inflammatory effects of MgSO4.

Methods: RAW264.7 cells, an immortalized murine macrophage-like cell line, were treated with phosphate buffered saline, MgSO4, lipopolysaccharide (LPS), LPS plus MgSO4, LPS plus MgSO4 plus extra-cellular supplement with calcium chloride (CaCl2), or LPS plus MgSO4 plus the L-type calcium channel activator BAY-K8644. After harvesting, the production of inflammatory molecules was evaluated. Because the production of endotoxin-induced inflammatory molecules is regulated by the crucial transcription factor nuclear factor (NF)-{kappa}B, we also evaluated the expression of NF-{kappa}B.

Results: LPS significantly induced the production of inflammatory molecules, including macrophage inflammatory protein-2, tumour necrosis factor-{alpha}, interleukin (IL)-1β, IL-6, nitric oxide/inducible nitric oxide synthase, and prostaglandin E2/cyclo-oxygenase-2. LPS also induced NF-{kappa}B activation, as inhibitor-{kappa}B degradation, NF-{kappa}B nuclear translocation, and NF-{kappa}B-DNA binding activity were significantly increased in LPS-treated RAW264.7 cells. MgSO4, in contrast, significantly inhibited the LPS-induced inflammatory molecules production and NF-{kappa}B activation. Moreover, the effects of MgSO4 on inflammatory molecules and NF-{kappa}B were reversed by extra-cellular calcium supplement with CaCl2 and L-type calcium channel activator BAY-K8644.

Conclusions: MgSO4 significantly inhibited endotoxin-induced up-regulation of inflammatory molecules and NF-{kappa}B activation in activated RAW264.7 cells. The effects of MgSO4 on inflammatory molecules and NF-{kappa}B may involve antagonizing calcium, inhibiting the L-type calcium channels, or both.

Keywords: enzymes, cyclo-oxygenase; intensive care; ions, ion channels, voltage-gated; ions, magnesium; nitric oxide


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