In genetically susceptible individuals, inflammatory bowel disease (IBD) is thought to occur because of an exaggerated immune response to normal intestinal flora with the contribution of multiple internal and external environmental factors. Many animal models are used to understand the pathophysiology and to develop new treatment modalities in this disease.The mechanisms that initiate inflammation in IBD are very variable. Toxin and infectious agents in the lumen cross the mucosal barrier and initiate inflammation in genetically susceptible individuals. Mucosal oxidative stress caused by inflammatory cells and disruption of redox balance plays a critical role in the pathogenesis of IBD. The production of reactive oxygen metabolites is accompanied by neutrophil infiltration and activation of colitis.

Thiamine (Vitamin B1) is an essential vitamin for organism metabolism. It is involved in the intermediate metabolism of carbohydrates in all body tissues. In thiamin deficiency, the use of pyruvic acid and some amino acids in tissues decreases, while the use of fats increases. Therefore, it is specifically required for the final metabolism of carbohydrates and many amino acids. Thiamin is synthesized in the colon and dietary intake. Thiamine pyrophosphate, the active form of thiamine, is an essential cofactor of five enzymes involved in glucose, amino acid, and lipid metabolism. Thiamin enables pro-apoptotic proteins of the Bcl-2 family, caspase-3 activation, and inhibition of poly- (ADP-ribose) polymerase (PARP) cleavage. It activates mitochondrial membrane potential, cytochrome c release, apoptosis-inducing factor, and then p38-MAPK, stress-activated kinases (SAPK / JNK), protein kinase C, and cytoplasmic phospholipase A2. Thiamin acting on macrophages has a potential anti-inflammatory and antioxidant effect by suppressing oxidative stress-induced NF-kappaB activation.

With Regards,
Sara Giselle
Associate Managing Editor
Global Journal of Digestive Diseases