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Monographs of fragrance chemicals and extracts that have caused contact allergy / allergic contact dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
A possible cross-reaction with salicyl alcohol has been observed, but this may also have been caused by simultaneous sensitization, as the causative allergenic material in this case, aspen bark, contained both chemicals (9).
Pharmacokinetic-Pharmacodynamic Correlations of Analgesics
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
In 1806, Sertürner reported the isolation of a pure substance in opium that he named morphine, after Morpheus, the Greek god of dreams. The discovery of other alkaloids in opium quickly followed that of morphine, for example, codeine by Robiquet in 1832 and papaverine by Merck in 1848. The background to aspirin goes back to antiquity to the early uses of decoctions or preparations of plants that contain salicylates. As early as AD 30, Celsius described the four classic signs of inflammation: redness, heat, pain, and swelling and he used extracts of willow leaves to relieve them. The first “clinical trial” on the use of willow bark in fever was reported by Edward Stone in 1763. Willow bark contains salicin, a glycoside of salicyl alcohol, which is metabolized in the body to salicylic acid, first discovered in 1829 by Leroux. Salicylic acid was prepared from salicin in 1838 by Piria and chemically synthesized in 1860 in Germany. Its ready supply led to even greater use as an external antiseptic, as an antipyretic, and in the treatment of rheumatism. Felix Hoffman, a scientist at Bayer, in attempts to reduce the bitter taste of salicylate, synthesized an acetylated form of salicylic acid in 1897 and in 1899 Dreser began the first pharmacological testing of acetyl salicylic acid, which was originally marketed by the Bayer company under the trade name of Aspirin, although this is now its generic name in most countries. About the same time, in 1893, acetaminophen was first introduced but was not used widely until 1949. There are many different possible modes of action of aspirin, but the one that has gained general recognition is through inhibition of prostaglandin biosynthesis by irreversible interaction with the enzyme cyclooxygenase.9 Beginning with indomethacin, several other reversible inhibitors of cyclooxygenase have now been introduced. Despite contrasting chemical structures these drugs are generally regarded as a group because of their similar therapeutic actions.
Salicin inhibits AGE-induced degradation of type II collagen and aggrecan in human SW1353 chondrocytes: therapeutic potential in osteoarthritis
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Salicin is a prodrug of acetylsalicylic acid, a main constituent of aspirin and can be derived from the stems and roots of Alangium chinense (Lour.) Harms. (Alangiaceae), a common evergreen shrub native to east and southeast Asia [1]. Alangium chinense has long been used in traditional Chinese medicine (TCM) to treat rheumatic disease, snake bites, circulatory issues, hemostasis, and toxicity, it is also used as a contraceptive or analgesic and to promote wound healing [2,3]. Records of the use of willow bark, another common source of salicylic acid, have been found dating back to the 3rd century B.C. [4]. Numerous substances can be derived from the rhizome, roots, stems, leaves, or flowers of Alangium chinense such as alkaloids, sugars, saponins, steroids, triterpenes, anthraquinones, and glycosides including salicin [2,5,6] Recently, research has focused on methods of extraction of salicin and its potential therapeutic applications [6–8] As a prodrug, salicin is hydrolyzed to salicyl alcohol and then oxidized to salicylic acid in the gut [9]. As a metabolite of salicin, salicylic acid inhibits the activity of cyclo-oxygenase (COX), which plays a major role in regulating pain, fever, and inflammation by metabolizing arachidonic acid, a prostaglandin precursor [10]. However, to the best of our knowledge, this is the first time that the potential effects of salicin have been explored in osteoarthritis (OA). OA is characterized by chronic inflammation and irreversible cartilage destruction, which takes a massive toll on patients’ quality of life and mobility. The main risk factor for OA is age, in part due to the accumulation of advanced glycation end-products (AGEs). AGEs came to exist in the body as a byproduct of the innate process of non-enzymatic glycation as well as via dietary intake, as AGEs are used as a food preservative owing to their high resilience to degradation [11,12]. Some of the factors involved in the development and progression of OA include oxidative stress, secretion of proinflammatory cytokines, recruitment of immune cells, degradation of cartilage and activation of proinflammatory signaling pathways, all of which are demonstrated to be triggered by exposure to AGEs.