THYMOL

The antioxidant properties of thymol have been well documented in various preclinical studies including cell lines and animal models. At high rate constants, it effectively scavenged the hydroxyl free radicals thereby producing major transient species named phenoxyl radicals. The generated adducts from the phenoxyl radicals undergo dehydration which can be accelerated by an alkaline medium. The addition of hydroxyl radicals at the ortho position (C6 atom) of the phenolic group yields the phenoxyl radical after dehydration. The attack at the ortho position is more favorable energetically while the attack at the para position is also expected to occur. Furthermore, additions at the ortho positions occur without any precomplex formation. The non-toxicity and redox potential of the thymol•/thymol couple makes

Thymol (150 μM) has been shown to ameliorate LPS-induced inflammation in murine macrophage cell lines (Chauhan et al., 2014). Thymol (84 μg/ml) treatment attenuated lipopolysaccharide (LPS) and interferon gamma (IFN-γ) induced macrophage inflammation in vitro by inhibiting messenger RNA expression of inducible nitric oxide (NO) in J774A.1 cell lines (Vigo et al., 2004). In human polymorphonuclear neutrophils (PMNs), thymol (10 and 20 μg/ml) inhibited the synthetic chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced release of elastase, a marker of inflammatory diseases and a serine proteinase released by activated human neutrophils in a concentration-dependent manner (Braga et al., 2006). Thymol (100 μM) has been reported to alter prostaglandin catalyzed biosynthesis by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM. These studies suggest the potential of thymol as an anti-inflammatory drug and indicate that it could be used in a similar fashion to non-steroidal anti-inflammatory drugs (Marsik et al., 2005).