What is colitis?
Colitis is inflammation of the inner lining of the colon and can be associated with diarrhea, abdominal pain,bloating, and blood in the stool. This inflammation may be due to a variety of reasons, including the following:
- infection,
- loss of blood supply to the colon,
- inflammatory bowel disease, and
- invasion of the colon wall with lymphocytic white blood cells or collagen.
Source:
http://www.medicinenet.com/colitis/article.htm
What is Irritable Bowel Syndrome?
Around one in five Australians experiences the unpleasant symptoms of irritable bowel syndrome (IBS) at some time. These include abdominal pain, mucus in the stools, and alternating diarrhoea and constipation. Other terms for irritable bowel syndrome include ‘spastic colon’ and ‘irritable colon’. It seems that people with IBS have sensitive bowels that are easily ‘upset’. More women than men are prone to IBS, and symptoms tend to first occur in early adulthood.
The cause is unknown, but environmental factors such as changes of routine, emotional stress, infection and diet can trigger an attack. Research has shown that the neurotransmitter serotonin may be important in the symptoms of IBS, by altering the function of nerve cells in the bowel and causing changes in pain sensation and bowel function.
Irritable bowel syndrome doesn’t cause lasting damage and doesn’t contribute to the development of serious bowel conditions, such as cancer or colitis.
The cause is unknown, but environmental factors such as changes of routine, emotional stress, infection and diet can trigger an attack. Research has shown that the neurotransmitter serotonin may be important in the symptoms of IBS, by altering the function of nerve cells in the bowel and causing changes in pain sensation and bowel function.
Irritable bowel syndrome doesn’t cause lasting damage and doesn’t contribute to the development of serious bowel conditions, such as cancer or colitis.
Symptoms of IBS
Some of the more common signs of irritable bowel syndrome include:
- Abdominal pain or cramping that is often relieved by passing wind or faeces
- Alternating diarrhoea and constipation
- A sensation that the bowels are not fully emptied after passing a motion
- Abdominal bloating
- Mucus present in the stools
- Nausea.
None of these symptoms are exclusive to IBS. It is unusual for IBS to produce these symptoms, for the first time, after the age of 40.
RiboCeine offers therapeutic benefit in Colitis and Irritable Bowel Disease (IBS)
Translational Research Volume 150, Issue 2, August 2007, Pages 122–129
Comparative efficacies of 2 cysteine prodrugs and a glutathione delivery agent in a colitis model
Herbert Nagasawa et al (VA Medical Center, Minneapolis)
Oxidant-mediated injury plays an important role in the pathophysiology of inflammatory bowel disease (IBD). Recently, antioxidants were shown to modulate colitis in mice. In this study, the protective effects of L-cysteine and glutathione (GSH) prodrugs are further evaluated against progression of colitis in a murine model. ICR mice were fed compounds incorporated into chow as follows: Group (A) received chow supplemented with vehicle. Group (B) was provided 2-(RS)-n-propylthiazolidine-4(R)-carboxylic-acid (PTCA), a cysteine prodrug. Group (C) received D-ribose-L-cysteine (RibCys), another cysteine prodrug that releases L-cysteine. Group (D) was fed L-cysteine-glutathione mixed sulfide (CySSG), a ubiquitous GSH derivative present in mammalian cells. After 3 days, the animals were further provided with normal drinking water or water supplemented with dextran sodium sulfate (DSS). Mice administered DSS developed severe colitis and suffered weight loss. Colonic lesions significantly improved in animals treated with PTCA and RibCys and, to a lesser extent, with CySSG therapy. Hepatic GSH levels were depleted in colitis animals (control vs DSS, P < 0.001), and normalized with prodrug therapies (control vs treatments,P > 0.05). Protein expressions of serum amyloid A and inflammatory cytokines [interleukin (IL)-6, IL-12, tumor necrosis factor-alpha (TNF-α), osteopontin (OPN)] were significantly increased in colitis animals and improved with therapies. Immunohistochemistry and Western blot analyses showed significant upregulation of the macrophage-specific markers, COX-2 and CD68, which suggests macrophage activation and infiltration in the colonic lamina propria in colitis animals. These abnormalities were attenuated in prodrug-treated mice.
In conclusion, these data strongly support the novel action of the PTCA against colitis, which further supports a possible therapeutic application for IBD patients.
Comparative efficacies of 2 cysteine prodrugs and a glutathione delivery agent in a colitis model
Herbert Nagasawa et al (VA Medical Center, Minneapolis)
Oxidant-mediated injury plays an important role in the pathophysiology of inflammatory bowel disease (IBD). Recently, antioxidants were shown to modulate colitis in mice. In this study, the protective effects of L-cysteine and glutathione (GSH) prodrugs are further evaluated against progression of colitis in a murine model. ICR mice were fed compounds incorporated into chow as follows: Group (A) received chow supplemented with vehicle. Group (B) was provided 2-(RS)-n-propylthiazolidine-4(R)-carboxylic-acid (PTCA), a cysteine prodrug. Group (C) received D-ribose-L-cysteine (RibCys), another cysteine prodrug that releases L-cysteine. Group (D) was fed L-cysteine-glutathione mixed sulfide (CySSG), a ubiquitous GSH derivative present in mammalian cells. After 3 days, the animals were further provided with normal drinking water or water supplemented with dextran sodium sulfate (DSS). Mice administered DSS developed severe colitis and suffered weight loss. Colonic lesions significantly improved in animals treated with PTCA and RibCys and, to a lesser extent, with CySSG therapy. Hepatic GSH levels were depleted in colitis animals (control vs DSS, P < 0.001), and normalized with prodrug therapies (control vs treatments,P > 0.05). Protein expressions of serum amyloid A and inflammatory cytokines [interleukin (IL)-6, IL-12, tumor necrosis factor-alpha (TNF-α), osteopontin (OPN)] were significantly increased in colitis animals and improved with therapies. Immunohistochemistry and Western blot analyses showed significant upregulation of the macrophage-specific markers, COX-2 and CD68, which suggests macrophage activation and infiltration in the colonic lamina propria in colitis animals. These abnormalities were attenuated in prodrug-treated mice.
In conclusion, these data strongly support the novel action of the PTCA against colitis, which further supports a possible therapeutic application for IBD patients.
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