By Kyle J. Norton
Colitis is a general term associated with the inflammation of the inner lining of the colon.
The disease can be caused by infection, inflammatory bowel disease (Crohn's disease (CD), ulcerative colitis(CD)), ischemic colitis, allergic reactions, and microscopic colitis.
Most cases of colitis are involved in the damage of the intestinal mucosal barrier, particularly to those of ulcerative colitis.
Epidemiologically, damage and a reduction of gut bacteria by dietary chemicals, such as antibiotics of the protective mucus layer and the underlying tissue by the poorly inactivated digestive proteases have been found to induce both UC and CD.
The intestinal mucosal barrier is the outermost layer of the lining of the intestines which plays an essential role to ensure the adequate containment of undesirable luminal contents within the intestine while preserving the ability to absorb nutrients.
Additionally, the intestinal mucosal barrier also processes various immunological mediators, including cytokines and chemokines stimulated by gut microbiota and host immune responses, thus maintaining a well-balanced relationship between gut microbes and the host immune system.
In other words, the intestinal mucosal barrier protects the colonic integrity by interacting with the gut microbiota and the immune response to prevent the inflammation of the colon that causes the onset of colitis.
Some researchers suggested disruption of the inaction of the immune system and gut microbiota caused by dysfunction of the intestinal mucosal barrier due to trauma, infection, neoplasia, and inflammation has been found to induce colitis in the experimental models.
Dr. K R Gardiner, the lead scientist in the examination of the mucosal barrier dysfunction as a feature of colitis irrespective of etiology or species wrote, "There were significantly increased systemic endotoxin concentrations in rats with acetic acid (7.5 (1.7-119.5) pg/ml), ethanol (13.7 (0-111.2) pg/ml), and hapten-induced (14.4 (5-31.1) pg/ml) colitis compared with saline controls (3.3 (0-13.7) pg/ml).
And, "There were significant correlations between the systemic endotoxin concentration and both the severity of colitis and of illness in acetic acid-induced colitis".
The finding strongly suggested that mucosal barrier dysfunction induces a significant increase in the chemical toxins involved in colitis development.
Betanin is a phytochemical in the class of red and yellow indole-derived pigments of Betacyanins, belonging to the group of Betalains, found abundantly in beets, chard, etc.
On finding a natural and bioactive compound with autophagy and anti-inflammation properties against the onset of colitis, researchers examined the effects of phytochemicals isolated from beetroot in an animal model.
The study included mice treated with intrarectal administration of 2,4,6-trinitrobenzenesulfonic acid (TNBS) (3.5 mg·20 g-1 ) induced colitis 2 or 4 days after treatment. Among the treated mice, some mice received trehalose (3% in drinking water 3 weeks before TNBS administration) or a daily administration of rapamycin (1.25 mg·kg-1, i.p.), betanin (1 g·kg-1, i.p.) or betanin + 3-methyladenine (3MA) (10 mg·kg-1, i.p.).
TNBS-treated mice alone showed impaired autophagy associated with body weight loss and intestinal damage.
Administration of trehalose, rapamycin, or betanin not only prevented the impaired autophagic flux induced by TNBS but also reduced the expression of pro-inflammatory cytokines in the intestinal mucosa.
The anti-inflammatory activity of trehalose, rapamycin, or betanin was also observed by a decrease in M1 macrophage markers.
The results suggested that betanin processes pharmacological stimulation of mucosal autophagy in reduced intestinal inflammation and improved murine colitis.
Furthermore, in patients with ulcerative colitis (UC) and Crohn's disease (CD). betanin also protected the colitic cells against oxidative DNA damage and induced apoptosis in neutrophils isolated from blood, through its antioxidant and anti-inflammatory properties.
The finding suggested that in normal intestinal cells, betanin protects the integrity of the cell against intestinal mucosal inflammation in the formation of colitis by inducing autophagy and anti-inflammatory effects.
Taken altogether, betanin used alone or combined with other herbal medicines may be considered supplements for the prevention and treatment of colitis, pending the confirmation of the larger sample size and multicenter human study.
Intake of betanin in the form of supplements should be taken with extreme care to prevent overdose acute liver toxicity.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right 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) Stimulation of autophagy prevents intestinal mucosal inflammation and ameliorates murine colitis by Macias-Ceja DC1, Cosín-Roger J2, Ortiz-Masiá D2,3, Salvador P2, Hernández C1,2, Esplugues JV1,2, Calatayud S2, Barrachina MD. (PubMed)
(2) DNA damage and apoptosis in blood neutrophils of inflammatory bowel disease patients and in Caco-2 cells in vitro exposed to betanin by Zielińska-Przyjemska M1, Olejnik A2, Dobrowolska-Zachwieja A3, Łuczak M4, Baer-Dubowska W. (PubMed)
(3) Colitis and colonic mucosal barrier dysfunction by K R Gardiner, N H Anderson, B J Rowlands, and A Barbul. (PMC)
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