Dehydrodiisoeugenol (DHIE) is a neolignan found in more than 17 plant species, including herbs, fruit, and root. DHIE was, for the first time, isolated from Myristica fragrans bark in 1973. Since then, many methodologies have been used for the obtention of DHIE, including classical chemistry synthesis using metal catalysts and biocatalytic synthesis; employing horseradish peroxidase; peroxidase from Cocos nucifera; laccase; culture cells of plants; and microorganisms. Increasing evidence has indicated that DHIE has a wide range of biological activities: anti-inflammatory, anti-oxidant, anti-cancerogenic, and anti-microbial properties. However, evidence in vivo and in human beings is still lacking to support the usefulness potential of DHIE as a therapeutic agent. This study’s review was created by searching for relevant DHIE material on websites such as Google Scholar, PubMed, SciFinder, Scholar, Science Direct, and others. This reviews the current state of knowledge regarding the different synthetical routes and biological applications of DHIE.

Background: Recent studies pointed up that curcumin produces an anti-nociceptive effect in inflammatory and neuropathic pain. However, the possible mechanisms of action that underline the anti-allodynic effect induced by curcumin are not yet established. The purpose of this study was to determine the possible anti-allodynic effect of curcumin in rats with L5-L6 spinal nerve ligation (SNL). Furthermore, we study the possible participation of the NO-cyclic GMP-ATP-sensitive K⁺ channels pathway in the anti-allodynic effect induced by curcumin. Methods: Tactile allodynia was measured using von Frey filaments by the up-down method in female Wistar rats subjected to SNL model of neuropathic pain. Results: Intrathecal and oral administration of curcumin prevented, in a dose-dependent fashion, SNL-induced tactile allodynia. The anti-allodynic effect induced by curcumin was prevented by the intrathecal administration of L-NAME (100 μg/rat, a non-selective nitric oxide synthase inhibitor), ODQ (10 μg/rat, an inhibitor of guanylate-cyclase), and glibenclamide (50 μg/rat, channel blocker of ATP-sensitive K⁺ channels). Conclusions: These data suggest that the anti-allodynic effect induced by curcumin is mediated, at least in part, by the NO-cyclic GMP-ATP-sensitive K⁺ channels pathway in the SNL model of neuropathic pain in rats.