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Antinociceptive Actions Of Honokiol And Magnolol On Glutamatergic And Inflammatory Pain

in vivo

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The antinociceptive effects of honokiol and magnolol, two major bioactive constituents of the bark

of Magnolia officinalis, were investigated on animal paw licking responses and thermal hyperalgesia

induced by glutamate receptor agonists including glutamate, N-methyl-D-aspartate (NMDA), and

metabotropic glutamate 5 receptor (mGluR5) activator (RS)-2-chloro-5-hydroxyphenylglycine

(CHPG), as well as inflammatory mediators such as substance P and prostaglandin E2 (PGE2) in

mice. The actions of honokiol and magnolol on glutamate-induced c-Fos expression in the spinal

cord dorsal horn were also examined. Our data showed that honokiol and magnolol blocked

glutamate-, substance P- and PGE2-induced inflammatory pain with similar potency and efficacy.

Consistently, honokiol and magnolol significantly decreased glutamate-induced c-Fos protein

expression in superficial (I-II) laminae of the L4-L5 lumbar dorsal horn. However, honokiol was

more selective than magnolol for inhibition of NMDA-induced licking behavioral and thermal

hyperalgesia. In contrast, magnolol was more potent to block CHPG-mediated thermal

hyperalgesia. These results demonstrate that honokiol and magnolol effectively decreased the

inflammatory pain. Furthermore, their different potency on inhibition of nociception provoked by

NMDA receptor and mGluR5 activation should be considered.



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