Pain & Inflammation

Nociception (pain perception) and inflammation are two responses of an organisms defence system towards external noxious stimuli. Although different in nature, pain and inflammation are strongly associated with each other. An important sign of inflammation - besides local redness, swelling, heat, and loss of function -  is in fact pain. The events of inflammation that underlie these symptoms are induced and regulated by a large number of chemical mediators that are also found to mediate the mechanisms of pain perception. These mediators include eicosanoids, kinins, complement proteins, neurotransmitters (e.g. histamine), protons, NO, prostaglandins, leukotrienes, neurotrophins, and monokines[1].
Inflammation is a major protective response of the immune system to tissue damage and infection, and ranges from the acute inflammation associated with infection of the skin, through to chronic inflammatory processes in atherosclerosis, asthma and chronic bronchitis, and rheumatoid arthritis, among many others. Acute inflammation is knows for its rapid onset and short duration. It is mediated by tissue-resident macrophages and mast cells, and characterized by the exudation of fluids and plasma proteins, and the migration of leukocytes (mainly neutrophils) into the injured area. In contrast, chronic inflammation is of a more prolonged duration and manifests histologically by the presence of lymphocytes and macrophages, resulting in fibrosis and tissue necrosis[2].
Similar to Inflammation, pain may also be divided into two main categories: acute and chronic pain. Acute or nociceptive pain is part of a rapid warning relay instructing the motor neurons of the central nervous system to minimize detected physical harm. It is mediated by nocicepters: free nerve endings that terminate just below the skin, in tendons, joints, and in body organs.  Nociceptors are extremely heterogeneous, differing in the neurotransmitters they contain, the receptors and ion channels they express, their speed of conduction, their response properties to noxious stimuli, and their capacity to be sensitized during inflammation, injury, and disease. Nociception can be associated with nerve damage caused by trauma, diseases such as diabetes, shingles, irritable bowel syndrome, late-stage cancer or the toxic effects of chemotherapy. It typically responds well to treatment with opioids and NSAIDs. Chronic pain, however, serves no biologic function as it is not a symptom of a disease process but is a disease process itself[3],[4].


[1] R. Medzhitov. Origin and physiological roles of inflammation. Nature 2008, 454, 428-435.
[2] E.O. Iwalewa et al. Inflammation: the foundation of diseases and disorders. A review of phytomedicines of South African origin used to treat pain and inflammatory conditions. Afr. J. Biotech. 2007, 6, 2868-2885.
[3] M. Percival. Understanding The Natural Management of Pain and Inflammation. Clin. Nutr. Insights 1999, 4, 1-5.
[4] C.L. Stucky et al. Mechanisms of pain. PNAS October 9, 2001, 98, 11845-11846.

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1915 A 803467 Blocker of the voltage-gated Nav1.8 channel €95.00
1113 AM 36 dihydrochloride Na+ channel blocker €145.00
2243 AVE 0118 hydrochloride Potassium channel blocker (Kv1.5 (IKur), Kv4.3 (Ito), Kir3.4 (IKAch), and IKr currents) €120.00
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1294 Chromanol 293B KCNQ1 channel blocker €95.00
2458 Clemizole Inhibitor of the transient receptor potential channel TRPC5 €75.00
1899 CNV 1014802 Na+ channel blocker; anti-convulsant €125.00
2548 CNV 1014802 hydrochloride Na+ channel blocker; anti-convulsant €125.00
1868 CRAC inhibitor 44 Potent and selective CRAC ion channel blocker €110.00
1322 DMP 543 K+ channel blocker; Ach release stimulator €90.00
2103 Dofetilide Kv11.1 (hERG) channel blocker €85.00
1448 Felodipine Ca2+ channel blocker €65.00
1735 Kv1.3 Channel blocker 42 Kv1.3 potassium channel blocker €110.00
1444 Lacosamide Na+ channel blocker; anti-convulsant €75.00
2423 M8-B hydrochloride Selective and potent antagonist of the TRPM8 channel €115.00

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