• Jeong Seon Cho, Tae Hoon Kim, Jae-Min Lim, and Jin-Ho Song.
• Department of Pharmacology, College of Medicine, Chung-Ang University, 221 Heuksuk-Dong, Dongjak-Ku, Seoul 156-756, Republic of Korea.
• Brain Res. 2008 Dec 3; 1243: 53-62.

AbstractEugenol is an aromatic molecule found in several plants and widely used in dentistry for analgesic and antiseptic purposes. It inhibits pro-inflammatory mediators including nitric oxide synthase, cyclooxygenase and lipoxygenase. It also regulates ion channels involved in pain signaling, such as TRPV1 receptor, high-voltage-activated Ca(2+) channels, NMDA receptor and GABA(A) receptor. The expression and functional properties of voltage-gated Na(+) channels in primary sensory neurons are altered following inflammation or nerve injury. To elucidate an involvement of Na(+) channels in the eugenol-induced analgesia we investigated the effects of eugenol on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) Na(+) currents in acutely dissociated rat dorsal root ganglion neurons. Eugenol inhibited TTX-S and TTX-R Na(+) currents in a concentration-dependent manner. The K(d) values were 308 muM and 543 muM, respectively. Eugenol did not influence the activation voltage of either type of Na(+) current. However, eugenol moved the steady-state inactivation curves of both Na(+) currents to a hyperpolarizing direction and reduced the maximal Na(+) current. Thus eugenol appears to inhibit Na(+) currents through its interaction with both resting and inactivated Na(+) channels. The recovery from inactivation of both Na(+) currents was slowed by eugenol. The eugenol inhibition of Na(+) currents was not dependent on the stimulus frequency. The inhibition of Na(+) currents is considered as one of the mechanisms by which eugenol exerts analgesia.

40 keywords...

hide…