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Anti-inflammatory refers to the property of a substance or treatment that reduces inflammation. Anti-inflammatory drugs make up about half of analgesics, remedying pain by reducing inflammation as opposed to opioids which affect the central nervous system.




Many steroids, specifically glucocorticoids, reduce inflammation or swelling by binding to cortisol receptors. These drugs are often referred to as corticosteroids.

Non-steroidal anti-inflammatory drugs

Non-steroidal anti-inflammatory drugs (NSAIDs), alleviate pain by counteracting the cyclooxygenase (COX) enzyme. On its own COX enzyme synthesizes prostaglandins, creating inflammation. In whole the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the pain.

Some common examples of NSAIDs are: aspirin, ibuprofen, and naproxen. The newer specific COX-inhibitors, although probably sharing a similar mode of action, are not classified together with the traditional NSAIDs.

On the other hand, there are analgesics that are commonly associated with anti-inflammatory drugs but that have no anti-inflammatory effects. An example is paracetamol, called acetaminophen in the U.S. and sold under the brand name of Tylenol. As opposed to NSAIDS, which reduce pain and inflammation by inhibiting COX enzymes, paracetamol has recently been shown to block the reuptake of endocannabinoids, which only reduces pain, likely explaining why it has minimal effect on inflammation.

Long-term use of NSAIDs can cause gastric erosions, which can become stomach ulcers and in extreme cases can cause severe haemorrhage resulting in death. The risk of death as a result of use of NSAIDs is 1 in 12,000 for young adults aged 16-45.[1] The risk increases almost twenty-fold for those over 75.[1] Other dangers of NSAIDs are exacerbating asthma and causing kidney damage.[1] Over use of acetaminophen (paracetamol) causes liver damage and is the most common cause of liver failure in the United States, according to a 2009 report from the federal Food and Drug Administration[2][3].

Immune Selective Anti-Inflammatory Derivatives (ImSAIDs)

ImSAIDs are a class of peptides being developed by IMULAN BioTherapeutics, LLC, which were discovered to have diverse biological properties, including anti-inflammatory properties. ImSAIDs work by altering the activation and migration of inflammatory cells, which are immune cells responsible for amplifying the inflammatory response.[4][5] The ImSAIDs represent a new category of anti-inflammatory and are unrelated to steroid hormones or non-steroidal anti-inflammatories.

The ImSAIDs were discovered by scientists evaluating biological properties of the submandibular gland and saliva. Early work in this area demonstrated that the submandibular gland released a host of factors which regulate systemic inflammatory responses and modulate systemic immune and inflammatory reactions. It is now well accepted that the immune, nervous and endocrine systems communicate and interact to control and modulate inflammation and tissue repair. One of the neuroendocrine pathways, when activated, results in the release of immune regulating peptides from the submandibular gland upon neuronal stimulation from sympathetic nerves. This pathway or communication is referred to as the cervical sympathetic trunk-submandibular gland (CST-SMG) axis, an regulatory system that plays a role in the systemic control of inflammation.[6]

Early work in identifying factors that played a role in the CST-SMG axis lead to the discovery of a seven amino acid peptide, called the submandibular gland peptide-T. SGP-T was demonstrated to have biological activity and thermoregulatory properties related to endotoxin exposure.[7] SGP-T, an isolate of the submandibular gland, demonstrated its immunoregulatory properties and potential role in modulating the cervical sympathetic trunk-submandibular gland (CST-SMG) axis, and subsequently was shown to play an important role in the control of inflammation.

One SGP-T derivative is a three amino acid sequence shown to be a potent anti-inflammatory molecule with systemic effects. This three amino acid peptide is phenylalanine-glutamine-glycine (FEG) and its D-isomeric form (feG), have become the foundation for the ImSAID category.[8] Cellular Effects of feG: The cellular effects of the ImSAIDs are characterized in a number of publications. feG and related peptides are known to modulate leukocyte (white blood cells) activity by influencing cell surface receptors to inhibit excessive activation and tissue infiltration.

One lead ImSAID, the tripeptide FEG (Phe-Glu-Gly) and its D-isomer feG are known to alter leukocyte adhesion involving actions on αMβ2 integrin, and inhibit the binding of CD16b (FCyRIII) antibody to human neutrophils.[9] feG has also been shown to decrease circulating neutrophil and eosinophil accumulation, decrease intracellular oxidative activity and reduced the expression of CD49d after antigen exposure.[10][11] [12]


In addition to medical drugs, some herbs may have anti-inflammatory qualities, including Harpagophytum, hyssop, ginger, Turmeric, Arnica montana which contains helenalin, a sesquiterpene lactone, and willow bark, which contains salicylic acid, the active ingredient in aspirin. Cannabichromene, one of the many cannabinoids present in the cannabis plant, has been shown to reduce inflammation.[13]

Possible benefits

Some clinical studies have suggested that a prolonged intake of certain anti-inflammatory (non-steroid) drugs may have a positive effect on Alzheimer. By contrast, anti-inflammatory treatment trials for existing Alzheimer have typically shown little to no effect on halting or reversing the disorder.[14][15] Research and clinical trials continue.[16]

Ice treatment

Applying ice, or even cool water, to a tissue injury has an anti-inflammatory effect and is often suggested as an injury treatment and pain management technique for athletes. One common approach is Rest, Ice, Comfortable Support and Elevation. Cool temperatures inhibit local blood circulation, which reduces swelling in the injured tissue.


Some advocate the consumption of anti-inflammatory foods as a means of controlling inflammation. A typical anti-inflammatory diet includes a well-balanced, varied diet that is high in vegetables and low in refined carbohydrates and undesirable fats, such as saturated fats and trans fats[17]. Anti-inflammatory foods include most colorful fruits and vegetables, oily fish (which contain higher levels of omega-3 fatty acids), nuts, seeds, and certain spices, such as ginger. Extra virgin olive oil contains a chemical oleocanthal that acts similarly to ibuprofen. Those following an anti-inflammatory diet will avoid refined oils and sugars, and show a preference for so-called anti-inflammatory foods in their meal choices.[18]

A diet high in vegetables and low in refined carbohydrates and saturated and trans fats may enhance the creation of prostaglandins. There are three main types of prostaglandins: PG-E1 and PG-E3, which have an anti-inflammatory properties, and PG-E2, which promotes inflammation.[19]


  1. ^ a b c NSAIDs and adverse effects at Bandolier, Table 7.
  2. ^
  3. ^
  4. ^ Bao F, John SM, Chen Y, Mathison RD, Weaver LC. The tripeptide phenylalanine-(D) glutamate-(D) glycine modulates leukocyte infiltration and oxidative damage in rat injured spinal cord. Neuroscience. 2006 Jul 7;140(3):1011-22. Epub 2006 Apr 3.
  5. ^ Mathison RD, Befus AD, Davison JS, Woodman RC. Modulation of neutrophil function by the tripeptide feG. BMC Immunol. 2003 Mar 4;4:3. Epub 2003 Mar 4
  6. ^ Mathison R, Davison JS, Befus AD. Neuroendocrine regulation of inflammation and tissue repair by submandibular gland factors. Immunol Today. 1994 Nov;15(11):527-32. Review.
  7. ^ Mathison RD, Malkinson T, Cooper KE, Davison JS. Submandibular glands: novel structures participating in thermoregulatory responses. Can J Physiol Pharmacol. 1997 May;75(5):407-13.
  8. ^ Dery RE, Mathison R, Davison J, Befus AD. Inhibition of allergic inflammation by C-terminal peptides of the prohormone submandibular rat 1 (SMR-1). Int Arch Allergy Immunol. 2001 an-Mar;124(1-3):201-4.
  9. ^ Mathison RD, Christie E, Davison JS. The tripeptide feG inhibits leukocyte adhesion. J Inflamm (Lond). 2008 May 20;5:6.
  10. ^ Dery RE, Ulanova M, Puttagunta L, Stenton GR, James D, Merani S, Mathison R, Davison J, Befus AD. Frontline: Inhibition of allergen-induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro-endocrine pathway. Eur J Immunol. 2004 Dec;34(12):3315-25
  11. ^ Mathison RD, Davison JS. The Tripeptide feG Regulates the Production of Intracellular Reactive Oxygen Species by Neutrophils. J Inflamm (Lond). 2006 Jun 15;3(1):9
  12. ^ Mathison R, Lo P, Tan D, Scott B, Davison JS. The tripeptide feG reduces endotoxin-provoked perturbation of intestinal motility and inflammation. Neurogastroenterol Motil. 2001 Dec;13(6):599-603.
  13. ^
  14. ^ Harv Ment Health Lett. 2008 Aug;25(2). Anti-inflammatory drugs may not protect cognitive function
  15. ^ Rogers J., J Periodontol. 2008 Aug;79(8 Suppl):1535-43. The inflammatory response in Alzheimer's disease'
  16. ^ Sano M, Grossman H, Van Dyk K, CNS Drugs. 2008;22(11):887-902, Preventing Alzheimer's disease : separating fact from fiction.
  17. ^
  18. ^ Hyman, Mark: "Ultra-Metabolism", page 137. Scribner, 2006
  19. ^ Anti-Inflammatory Diet To Fight Silent Inflammation

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