Kyle J. Norton
Inflammation is a natural defense of the immune system that protects the body against the invasion of harmful stimuli and pathogens.
Anti-inflammatory activity is the process of reducing inflammation or swelling without affecting the function of the immune system.
In the acute phase of infection, the immune first line of defense, the white blood cells, macrophages stimulates the production of blood platelets to cover the wound or cut and proinflammatory cytokines to destroy all invaders.
Most cases of acute infection are stopped at this phase and the wound is healed quickly.
However, if the wound is too large, then the recovery may take a longer period and through 4 overlap recovery stages. Any interruption in the overlapped recover stage may cause the formation of scars.
Moreover, overproduction of proinflammatory cytokines that kills harmful pathogens may cause damage and death of nearby healthy cells, leading to the formation of scars, such as scar in the liver caused by hepatitis infection.
Additionally, if the immune system can not destroy the invasive pathogens in a set of times, it will compromise, leading to low-grade inflammation. Prolonged low-grade inflammation caused by continuing the production of pro-inflammatory cytokines can result in serious and chronic diseases.
Diseases associated with chronic inflammation induced by protein, lipid and cellular damage include cardiovascular disease, diabetes, neurodegenerative disease,... and cancers.
The results have been found to cause cell death and alternation of cell DNA.
In finding a potent compound that processes anti-inflammatory property, researchers investigated the activity of indicaxanthin, in an animal model of acute inflammation.
According to the tested differentiation of rats induced by injection of 0.2 mL of λ-carrageenin in the pleural cavity pretreated by indicaxanthin at 2 μmol/kg,
* Pretreatment of the phytochemical inhibited the release of pro-inflammatory PGE(2) (91.4%), NO (67.7%), IL-1β (53.6%), and TNF-α (71.1%) induced by carrageenan-induced rats.
* Furthermore, enzymes and proteins associated with the production of proinflammatory cytokines such as IL-1β (34.5%), TNF-α (81.6%), iNOS (75.2%), and COX2 (87.7%) mRNA were also inhibited by the pretreatment of indicaxanthin.
* iNOS (71.9%) and COX-2 (65.9%) enzyme expressions involved in the inflammatory processes that recruit the leukocytes are also inhibited by the bioactive compound.
* Moreover, enzymes associated with the induction of free radicals chain reaction were also curbed by the indicaxanthin at a time- and dose-dependently.
Pharmacokinetically, the most efficacy in inhibition of inflammation was found to have a maximum 0.22 ± 0.02 μmol/L (n = 15) plasma concentration of indicaxanthin, with a half-life of 1.15 ± 0.11 h.
Based on the findings, researchers said, "This dietary pigment has the potential to improve health and prevent inflammation-based disorders".
Taken together, indicaxanthin may be considered a remedy for the prevention and treatment of inflammation, pending the confirmation of the larger sample size and multicenter human study.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All rights reserved)
Health article writer and researcher; Over 10,000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, Best Before it's news, the karate GB Daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for Shorty Award over last 4 years
Some articles have been used as references in medical research, such as the international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Indicaxanthin from cactus pear fruit exerts anti-inflammatory effects in carrageenin-induced rat pleurisy by Allegra M1, Ianaro A, Tersigni M, Panza E, Tesoriere L, Livrea MA. (PubMed)
(2) Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells by Tesoriere L1, Attanzio A1, Allegra M1, Gentile C1, Livrea MA. (PubMed)
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