Inflammation with phenol treatment

Other Systemic Effects. Direct application of phenol to the tympanic membrane in the ear of rats resulted in inflammation (Schmidt and Hellstrom 1993). When phenol was placed in the ear of rats after tympanic membrane puncture, inflammation and a reduction in auditory brainstem response were observed (Schmidt et al. 1990). These studies indicate that direct application of phenol to the ear for treatment of ear infection should be used with caution. 

The use of Fraxinus ornus bark in the Bulgarian folk medicine for treatment of inflammation, arthritis and dysentery [1,2] suggests the presence of some active principles with anti-inflammatory activity. Our phytochemical investigations have shown that the bark contains hydroxycoumarins, secoiridoid glucosides, caffeoyl esters of phenylethanoid glycosides and other phenolic compounds [10,14-17,28]. RP-HPLC analysis of commercial samples of Fraxinus ornus bark revealed high esculin (1) content (6-9%) [14]. 

B. Specific drugs and antidotes. For most agents, there Is no specific antidote. (See p 221 for hydrofluoric acid bums and p 302 for phenol bums.) In the past, corticosteroids were used by many clinicians in the hope of reducing scarring, but this treatment has been proved ineffective. Moreover, steroids may be harmful in the patient with perforation because they mask early signs of inflammation and inhibit resistance to infection. 

Caffeic Acid Phenethyl Ester (CAPE). CAPE, a phenolic compound with antioxidant properties, is an active ingredient derived from honeybee propolis (52). CAPE has antiviral, anti-inflammatory and antiproliferative properties. The compound differentially suppresses the growth of numerous human cancer cells and also inhibits tumor promoter-mediated processes in transformed cells (53,54). In transformed cells, CAPE induces apoptosis and inhibits the expression of the malignant phenotype (55,56). In addition, CAPE treatment attenuates the formation of azoxymethane-induced aberrant crypts and the activities of ornithine decarboxylase (ODC), tyrosin protein kinase, and lipoxygenase activity (57). Although the molecular basis for these multiple chemopreventive effects of CAPE is not clear, recent studies have demonstrated that CAPE is a potent and specific inhibitor of the transcription factor NF-kB (58). CAPE inhibited the activity and expression of COX-2 in the carrageenan air pouch model of inflammation as well as in TPA-treated human oral epithelial cells (59). CAPE was able to reduce neointimal formation by inhibiting NF-kB activation in a model of endothelial injury of rat carotid artery (60). 

Aspirin, prepared industrially by selective electrophilic aromatic substitution of phenol, is arguably the blockbuster drug of all times. Its active metabolite, 2-hydroxybenzoic acid (salicylic acid), obtained from the bark of the white willow tree, has been used for four millennia for the treatment of inflammation and to relieve pain or discomfort caused by arthritis, soft-tissue injuries, and fever. Aspirin was discovered by the German company Bayer in the late 19th century and ironically marketed together with another drug, heroin, whose addictive side effects were not recognized then. 

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