Mesenteric ischemia encompasses a range of clinical syndromes resulting from structural damage and dysfunction of the intestines due to inadequate blood perfusion or obstruction of blood flow. Treatment options typically include thrombolytic therapy, interventional procedures, and surgical interventions. Colitis, on the other hand, refers to inflammatory lesions in the colon triggered by pathogens, allergic reactions, and various physical and chemical factors. Treatment strategies primarily focus on suppressing the inflammatory response, modulating immune function, and providing individualized and comprehensive symptomatic care. Prior research has demonstrated the advantageous effects of preserving NAD+ homeostasis on a range of intestinal disorders, including mesenteric ischemia and colitis. NAD+ and its precursors have been shown to mitigate oxidative stress, inflammation, and apoptosis in models of intestinal diseases by modulating the functions of NAD+-dependent deacetylases such as sirtuins, PARP, and CD38. This regulation ultimately leads to a decrease in intestinal damage and the maintenance of intestinal homeostasis.

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Coenzyme I and Intestinal Diseases

  • Shan-Yao Pan,
  • Li Luo

摘要

Mesenteric ischemia encompasses a range of clinical syndromes resulting from structural damage and dysfunction of the intestines due to inadequate blood perfusion or obstruction of blood flow. Treatment options typically include thrombolytic therapy, interventional procedures, and surgical interventions. Colitis, on the other hand, refers to inflammatory lesions in the colon triggered by pathogens, allergic reactions, and various physical and chemical factors. Treatment strategies primarily focus on suppressing the inflammatory response, modulating immune function, and providing individualized and comprehensive symptomatic care. Prior research has demonstrated the advantageous effects of preserving NAD+ homeostasis on a range of intestinal disorders, including mesenteric ischemia and colitis. NAD+ and its precursors have been shown to mitigate oxidative stress, inflammation, and apoptosis in models of intestinal diseases by modulating the functions of NAD+-dependent deacetylases such as sirtuins, PARP, and CD38. This regulation ultimately leads to a decrease in intestinal damage and the maintenance of intestinal homeostasis.