4.3 Article

Dextran sodium sulfate alters antioxidant status in the gut affecting the survival of Drosophila melanogaster

Journal

3 BIOTECH
Volume 12, Issue 10, Pages -

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s13205-022-03349-2

Keywords

Drosophila; Dextran sodium sulfate; Antioxidant; Smurfing; Inflammatory bowel disease

Funding

  1. UGC-SAP

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Inflammatory bowel disease (IBD), characterized by chronic inflammation in the intestine, is triggered by oxidative stress caused by reactive free radicals. The global incidence of IBD is increasing but lacks long-term therapeutic options. The absence of adequate animal models has hindered understanding the pathogenesis of IBD. This study used Drosophila as a model to induce and investigate DSS-induced colitis, finding that DSS-induced inflammation in Drosophila lowers antioxidant molecule levels, affects lifespan, and induces cellular damage in the GI tract.
Inflammatory bowel disease (IBD) is a group of disorders characterized by chronic inflammation in the intestine. Several studies confirmed that oxidative stress induced by an enormous amount of reactive free radicals triggers the onset of IBD. Currently, there is an increasing trend in the global incidence of IBD and it is coupled with a lack of adequate long-term therapeutic options. At the same time, progress in research to understand the pathogenesis of IBD has been hampered due to the absence of adequate animal models. Currently, the toxic chemical Dextran Sulfate Sodium (DSS) induced gut inflammation in rodents is widely perceived as a good model of experimental colitis or IBD. Drosophila melanogaster, a genetic animal model, shares similar to 75% sequence similarity to genes causing different diseases in humans and also has conserved digestion and absorption features. Therefore, in the current study, we used Drosophila as a model system to induce and investigate DSS-induced colitis. Anatomical, biochemical, and molecular analyses were performed to measure the levels of inflammation and cellular disturbances in the gastrointestinal (GI) tract of Drosophila. Our study shows that DSS-induced inflammation lowers the levels of antioxidant molecules, affects the life span, reduces physiological activity and induces cellular damage in the GI tract mimicking pathophysiological features of IBD in Drosophila. Such a DSS-induced Drosophila colitis model can be further used for understanding the molecular pathology of IBD and screening novel drugs.

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