FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Keshav, N., Ammankallu, R., Shashidhar, , Paithankar, J.G., Baliga, M.S., Patil, R.K., Kudva, A.K., Raghu, S.V. (2022). Dextran sodium sulfate alters antioxidant status in the gut affecting the survival of Drosophila melanogaster.  3 Biotech 12(10): 280.
FlyBase ID
FBrf0254787
Publication Type
Research paper
Abstract
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 ~ 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.
PubMed ID
PubMed Central ID
PMC9481858 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    3 Biotech
    Title
    3 Biotech
    ISBN/ISSN
    2190-5738 2190-572X
    Data From Reference
    Chemicals (1)
    Genes (5)
    Human Disease Models (1)