Pleiotropic Effects of Eugenol: The Good, the Bad, and the Unknown

Abstract

Phytocompounds and medicinal herbs were used in traditional ancient medicine and are nowadays increasingly screened in both experimental and clinical settings due to their beneficial effects in several major pathologies. Similar to the drug industry, phytotherapy is interested in using nanobased delivery systems to view the identification and characterization of the cellular and molecular therapeutic targets of plant components. Eugenol, the major phenolic constituent of clove essential oil, is a particularly versatile phytochemical with a vast range of therapeutic properties, among which the anti-inflammatory, antioxidant, and anticarcinogenic effects have been systematically addressed. In the past decade, with the emerging understanding of the role of mitochondria as critical organelles in the pathophysiology of noncommunicable diseases, research regarding the role of phytochemicals as modulators of bioenergetics and metabolism is on a rise. Here, we present a brief overview of the major pharmacological properties of eugenol, with special emphasis on its applications in dental medicine, and provide preliminary data regarding its effects, alone, and included in polyurethane nanostructures, on mitochondrial bioenergetics, and glycolysis in human HaCaT keratinocytes.

Figure 1

The time-dependency of HaCaT cell viability. (EU: free eugenol; P: polyurethane nanostructure alone; EU + P: eugenol included as nanoformulation). Data are presented as mean ± SD. Experiments were performed in triplicate (^∗p < 0.05 vs. Ctrl).

Figure 2

The effects of compounds (50 μM) on HaCaT cell migration. (EU: free eugenol, P: polyurethane nanostructure alone, EU + P: eugenol included as nanoformulation). Pictures were taken at 0, 3, and 24 h poststimulation (10× magnification).

Figure 3

The effects of 24 h incubation of HaCaT cells on OCR and ECAR. Data are presented as mean ± SD. Experiments were performed in triplicate.

Figure 4

The effects of 48 h incubation of HaCaT cells on OCR and ECAR. Data are presented as mean ± SD. Experiments were performed in triplicate (^∗∗∗p < 0.001 vs. Ctrl).

Figure 5

The effects of 72 h incubation of HaCaT cells on OCR and ECAR. Data are presented as mean ± SD. Experiments were performed in triplicate (^∗p < 0.05; ^∗∗p < 0.01; ^∗∗∗p < 0.001 vs. Ctrl).