Anti-inflammatory

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

Non-steroidal anti-inflammatory drugs[edit]

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 are not classified together with the traditional NSAIDs even though they presumably share the same mode of action.

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 (known as acetaminophen in the U.S). As opposed to NSAIDs, which reduce pain and inflammation by inhibiting COX enzymes, paracetamol has - as early as 2006 - been shown to block the reuptake of endocannabinoids,[1][2] which only reduces pain, likely explaining why it has minimal effect on inflammation.

Side-effects[edit]

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 GI bleeding caused by the use of NSAIDs is 1 in 12,000 for adults aged 16–45.[3] The risk increases almost twentyfold for those over 75.[3] Other dangers of NSAIDs are exacerbating asthma and causing kidney damage.[3] Apart from aspirin, prescription and over-the-counter NSAIDs also increase the risk of myocardial infarction and stroke.[4]

Therefore, the best NSAIDs would be those that neither cause gastric erosions nor increase the risk of myocardial infarction and stroke.[citation needed] At this time, no such agent is licensed for use in the US.

Immune selective anti-inflammatory derivatives (ImSAIDs)[edit]

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.[5][6] 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 that 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, a regulatory system that plays a role in the systemic control of inflammation.[7]

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.[8] 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.[9] 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.[10] feG has also been shown to decrease circulating neutrophil and eosinophil accumulation, decrease intracellular oxidative activity, and reduce the expression of CD49d after antigen exposure.[11][12][13]

Bioactive compounds[edit]

Many bioactive compounds showed anti-inflammatory activities on albino rat. Anti-inflammatory activity of Plumbago zylanica consists of Bioactive compound Plumbagin showed high activity in very low concentration.[14] More recently plumericin from the Amazonian plant Himatanthus sucuuba has been described as a potent anti-inflammatory agent in vitro and in vivo.[15]

Long-term effects[edit]

Anti-inflammatory treatment trials for existing Alzheimer's disease have typically shown little to no effect on halting or reversing the disease.[16][17] Research and clinical trials continue.[18] Two studies from 2012 and 2013 found regular use of aspirin for over ten years is associated with an increase in the risk of macular degeneration.[19][20]

Ice treatment[edit]

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, compression and elevation. Cool temperatures inhibit local blood circulation, which reduces swelling in the injured tissue.

Health supplements[edit]

In addition to medical drugs, some herbs and health supplements may have anti-inflammatory qualities: bromelain from pineapples (Ananas comosus).[21] Cannabichromene, a cannabinoid, also has anti-inflammatory effect.[22] Honokiol from Magnolia inhibits platelet aggregation, and works as an inverse agonist at the CB2 receptor. Black seed (Nigella sativa) has shown anti-inflammatory effect due to its high thymoquinone content.[23] St. John's wort's chief constituent, hyperforin, has been found to be a potent COX-1 and 5-LO inhibitor, with anti-inflammatory effect several fold that of aspirin.[citation needed]

Anti-inflammatory foods[edit]

Prostaglandins are hormone-like substances that affect the body in variety of ways, also regulating inflammatory mediation. An anti-flammatory diet includes fewer foods that create inflammation-causing prostaglandins (PGE2) in the body, and more foods that create anti-inflammatory prostaglandins (PGE1 and PGE3).[24][not in citation given]

Suggested diets to reduce inflammation include those rich in vegetables and low in simple carbohydrates and fats, such as saturated fats and trans fats.[25] 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, garlic and cayenne. Extra-virgin olive oil contains the 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.[26][27]

Omega-3 fatty acids have been shown to disrupt inflammation cell signaling pathways by binding to the GPR120 receptor.[28]

Measurement of dietary inflammation[edit]

The Dietary Inflammatory Index (DII) is a score (number) that describes the potential of diet to modulate systemic inflammation within the body. Until the creation of the DII by scientists led by Dr. James R. Hébert at the Statewide South Carolina Cancer Prevention and Control Program in the University of South Carolina, no indicator of diet-related inflammation had ever been devised. The DII has been subjected to construct validation, which tested (and subsequently confirmed) its ability to predict blood levels of inflammatory markers.

Exercise[edit]

Developing research has demonstrated that many of the benefits of exercise are mediated through the role of skeletal muscle as an endocrine organ. That is, contracting muscles release multiple substances known as myokines which promote the growth of new tissue, tissue repair, and various anti-inflammatory functions, which in turn reduce the risk of developing various inflammatory diseases.[29]

References[edit]

  1. ^ Ottani, Alessandra; Leone, Sheila; Sandrini, Maurizio; Ferrari, Anna; Bertolini, Alfio (February 15, 2006). "The analgesic activity of paracetamol is prevented by the blockade of cannabinoid CB1 receptors". European Journal of Pharmacology. 531 (1-3): 280–281. doi:10.1016/j.ejphar.2005.12.015. PMID 16438952. 
  2. ^ Dani, Mélina; Guindon, Josée; Lambert, Chantal; Beaulieu, Pierre (November 14, 2007). "The local antinociceptive effects of paracetamol in neuropathic pain are mediated by cannabinoid receptors". European Journal of Pharmacology. 573 (1-3): 214–215. doi:10.1016/j.ejphar.2007.07.012. PMID 17651722. 
  3. ^ a b c "Table 7". NSAIDs and adverse effects. Bandolier. Retrieved December 20, 2012. 
  4. ^ Trelle, Sven; Reichenbach, Stephan; Wandel, Simon; Hildebrand, Pius; Tschannen, Beatrice; Villiger, Peter M.; Egger, Matthias; Jüni, Peter (11 January 2011). "Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis". British Medical Journal (Clinical research ed.). 342: c7086. doi:10.1136/bmj.c7086. PMC 3019238Freely accessible. PMID 21224324. 
  5. ^ Bao, F.; John, S.M.; Chen, Y.; Mathison, R.D.; Weaver, L.C. (2006). "The tripeptide phenylalanine-(d) glutamate-(d) glycine modulates leukocyte infiltration and oxidative damage in rat injured spinal cord". Neuroscience. 140 (3): 1011–1022. doi:10.1016/j.neuroscience.2006.02.061. PMID 16581192. 
  6. ^ Mathison, Ronald D.; Befus, A. Dean; Davison, Joseph S.; Woodman, Richard C. (2003). "Modulation of neutrophil function by the tripeptide feG". BMC Immunology. 4 (3): 3. doi:10.1186/1471-2172-4-3. PMC 152650Freely accessible. PMID 12659660. Retrieved December 20, 2012. 
  7. ^ Mathison, R.; Davison, J.S.; Befus, A.D. (November 1994). "Neuroendocrine regulation of inflammation and tissue repair by submandibular gland factors". Immunology Today. 15 (11): 527–532. doi:10.1016/0167-5699(94)90209-7. PMID 7802923. 
  8. ^ Mathison, Ronald D.; Malkinson, Terrance; Cooper, K.E.; Davison, J.S. (1997). "Submandibular glands: novel structures participating in thermoregulatory responses". Canadian Journal of Physiology and Pharmacology. 75 (5): 407–413. doi:10.1139/y97-077. PMID 9250374. 
  9. ^ Dery, R.E.; Mathison, R.; Davison, J.; Befus; A.D. (2001). "Inhibition of allergic inflammation by C-terminal peptides of the prohormone submandibular rat 1 (SMR-1)". International archives of allergy and immunology. 124 (1–3): 201–024. doi:10.1159/000053710. PMID 11306968. 
  10. ^ Mathison, Ronald D; Christie, Emily; Davison, Joseph S (1 January 2008). "The tripeptide feG inhibits leukocyte adhesion". Journal of Inflammation. 5 (1): 6. doi:10.1186/1476-9255-5-6. PMC 2408570Freely accessible. PMID 18492254. 
  11. ^ Dery, René E.; Ulanova, Marina; Puttagunta, Lakshmi; Stenton, Grant R.; et al. (2004). "Frontline: Inhibition of allergen-induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro-endocrine pathway". European Journal of Immunology. 34 (12): 3315–3325. doi:10.1002/eji.200425461. PMID 15549777. 
  12. ^ Mathison, Ronald D.; Davison, Joseph S. (2006). "The tripeptide feG regulates the production of intracellular reactive oxygen species by neutrophils". Journal of Inflammation. 3 (9): 9. doi:10.1186/1476-9255-3-9. PMC 1534017Freely accessible. PMID 16776845. Retrieved December 20, 2012. 
  13. ^ Mathison, R.; Lo, P.; Tan, D.; Scott, B.; Davison, J. S. (2001). "The tripeptide feG reduces endotoxin-provoked perturbation of intestinal motility and inflammation". Neurogastroenterology & Motility. 13 (6): 599–603. doi:10.1046/j.1365-2982.2001.00294.x. PMID 11903921. 
  14. ^ Poul B.N.; Mukadam D.S.; Dama L.B. Dama (1999). "Anti-inflammatory activity of Plumbago zylanica". Fronteries Bot. 1: 91–93. 
  15. ^ Fakhrudin, N.; Waltenberger, B.; Cabaravdic, M.; Atanasov, AG.; et al. (April 2014). "Identification of plumericin as a potent new inhibitor of the NF-κB pathway with anti-inflammatory activity in vitro and in vivo.". Br J Pharmacol. 171 (7): 1676–86. doi:10.1111/bph.12558. PMID 24329519. 
  16. ^ "Anti-inflammatory drugs may not protect cognitive function". Harvard Mental Health Letter. 25 (2): 7. August 2008. PMID 18724438. 
  17. ^ Rogers, Joseph (2008). "The Inflammatory Response in Alzheimer's Disease". Journal of Periodontology. 79 (8 Supplement): 1535–1543. doi:10.1902/jop.2008.080171. PMID 18673008. 
  18. ^ Sano, M.; Grossman, H.; Van Dyk, K. (2008). "Preventing Alzheimer's disease: separating fact from fiction.". CNS Drugs. 22 (11): 887–902. doi:10.2165/00023210-200822110-00001. PMID 18840031. 
  19. ^ Liew, G.; Mitchell, P.; Wong, T. Y.; Rochtchina, E.; Wang, J. J. (2013). "The Association of Aspirin Use with Age-Related Macular Degeneration". JAMA Internal Medicine. 173 (4): 1–7. doi:10.1001/jamainternmed.2013.1583. PMID 23337937. 
  20. ^ Klein, B. E. K.; Howard, K. P.; Gangnon, R. E.; Dreyer, J. O.; Lee, K. E.; Klein, R. (2012). "Long-term Use of Aspirin and Age-Related Macular Degeneration". JAMA: the Journal of the American Medical Association. 308 (23): 2469–2478. doi:10.1001/jama.2012.65406. PMID 23288416. 
  21. ^ Akhtar, N.; Haqqi, T. M. (2012). "Current nutraceuticals in the management of osteoarthritis: A review". Therapeutic Advances in Musculoskeletal Disease. 4 (3): 181–207. doi:10.1177/1759720X11436238. PMC 3400101Freely accessible. PMID 22850529. 
  22. ^ Turner, Carlton, E.; Elsohly, Mahmoud A. (1981). "Biological activity of cannabichromene, its homologs and isomers" (PDF). Journal of Clinical Pharmacology. 21 (8–9 Supplement): 283S–291S. doi:10.1002/j.1552-4604.1981.tb02606.x. PMID 7298870. Retrieved December 20, 2012. 
  23. ^ Alemi, M.; Sabouni, F.; Sanjarian, F.; Haghbeen, K.; Ansari, S. (2012). "Anti-inflammatory Effect of Seeds and Callus of Nigella sativa L. Extracts on Mix Glial Cells with Regard to Their Thymoquinone Content". AAPS PharmSciTech. 14 (1): 160–7. doi:10.1208/s12249-012-9899-8. PMID 23255199. 
  24. ^ "Inflammation". Southern California College of Optometry. Retrieved 29 January 2013. [unreliable medical source?]
  25. ^ "Dr. Weil's Anti-Inflammatory Food Pyramid". Dr Weil. Retrieved December 20, 2012. [unreliable medical source?]
  26. ^ "List of 63 Anti-Inflammatory Foods to Choose from for Natural Healing". The Natural Anti-Inflammatory Remedies. Retrieved December 20, 2012. [unreliable medical source?]
  27. ^ Hyman, Mark (2006). Ultrametabolism: The Simple Plan for Automatic Weight Loss. New York, New York: Simon and Schuster. p. 137. ISBN 9781416531821. Retrieved December 20, 2012. [unreliable medical source?]
  28. ^ Willyard, Cassandra (September 2, 2010). "How Fish Oil Fights Inflammation". ScienceNOW. Retrieved December 20, 2012. 
  29. ^ Pedersen, BK. (Jul 2013). "Muscle as a secretory organ.". Compr Physiol. 3 (3): 1337–62. doi:10.1002/cphy.c120033. PMID 23897689. 
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