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Fig. 2. Proposed mechanism of action for the neuroprotective effect of naloxone. By
inhibiting the LPS-stimulated release of neurotoxic factors such as cytokines TNF-
and IL-1
and free radicals such as NO and superoxide, naloxone affords protection to
dopaminergic neurons against infl ammation-mediated degeneration.
true that inhibition of neutrophil activation alone may not be suffi cient to reverse
the course of the catastrophic cascade of the multiorgan failures
(23
,
81)
.
In animal studies and clinical trials, (-)-naloxone has a relatively large safety
margin. (+)-Naloxone, devoid of opioid activity, would be a better choice as a
candidate agent for potential use in the treatment of neurodegenerative diseases
such as PD and infl ammation-related disorders in general.
References
1. Smith, A. P. and Lee, N. M. (1988) Pharmacology of dynorphin.
Annu. Rev.
Pharmacol. Toxicol.
28,
123-140.
2. Herz, A. (1993)
Opioids
, Vol. 1. Springer-Verlag, Berlin.
3. Barron, B. A. (2000) Cardiac opioids.
Proc. Soc. Exp. Biol. Med.
224,
1-7.
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