Ulcerative colitis, pathophysiological mechanisms and drug repurposing: a new therapeutic dawn-narrative review

Crohn's disease and ulcerative colitis (UC) are among the intestinal conditions that make up the category known as inflammatory bowel disease. Globally, UC prevalence and incidence are currently rising. There was substantial evidence that many pathways were involved in the pathophysiology of UC. Of these pathways, interleukin 6 (IL-6)/signal transducer and activator of transcription 3 (STAT3), mammalian target of rapamycin and AMP-activated protein kinase (AMPK), Sphingosine kinase (SPHK)/ Sphingosine-1-phosphate, nuclear factor erythroid-2 related factor 2 (Nrf2)/heme oxygenase (HO-1). While small-molecule pharmaceuticals and biologics are available to treat patients with UC, approximately one-third of people receiving treatment do not get better. To find an effective remedy for UC patients, new therapy and medication repurposing have therefore been thoroughly researched. Several medications, including rosiglitazone, amlodipine, felodipine, atorvastatin, metformin, pentoxifylline, nitazoxanide, nifuroxazide, carbocisteine, levetiracetam, topiramate, nicodamid, and vildagliptin, have been shown to have positive effects on multiple organs through their anti-inflammatory properties. Furthermore, data on gut barrier integrity, oxidative stress, and inflammatory pathways showed that these medications had a major favorable impact on these parameters in both cellular and clinical models of UC. Using the findings of in vitro, in vivo, and clinical investigations, the positive effects of these medications on UC are thoroughly outlined and examined in the present research. Having a better knowledge of these protective benefits and the basic mechanisms may make it possible for UC patients to take these medications effectively.