Dihydroartemisinin attenuates acetic acid-induced ulcerative colitis in rats: Suppression of inflammation and modulation of NFκβ/TNF-α/RIPK1-mediated necroptosis and apoptosis

  • 0Department of Basic Medical Sciences, College of Medicine, AlMaarefa University, P.O.Box 71666, Riyadh 11597, Saudi Arabia; Department of Anatomy and Embryology, Faculty of Medicine, Mansoura University, Mansoura 35516, Egypt.

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Summary

This summary is machine-generated.

Dihydroartemisinin (DHA) effectively treats ulcerative colitis (UC) in rats by reducing oxidative stress and inflammation. DHA also modulates key proteins in cell death pathways, offering a potential new therapy for UC.

Area Of Science

  • Gastroenterology
  • Pharmacology
  • Cell Biology

Background

  • Ulcerative colitis (UC) involves oxidative stress and inflammation.
  • Dihydroartemisinin (DHA) possesses anti-inflammatory and antioxidant properties.

Purpose Of The Study

  • To evaluate DHA's therapeutic effects on acetic acid-induced UC in rats.
  • To investigate DHA's impact on anti-inflammatory and necroptotic pathways (NFκB/TNF-α/RIPK1).

Main Methods

  • Acetic acid-induced colitis model in rats.
  • Assessment of histological, biochemical, and molecular markers.
  • DHA administered via intraperitoneal injection.

Main Results

  • DHA reduced UC severity, inflammation, and oxidative stress markers (MDA, TNF-α, IL-6).
  • DHA increased antioxidant (GSH) and anti-inflammatory (IL-10) markers.
  • DHA downregulated key proteins in apoptotic and necroptotic pathways (TNF-α, RIPK1, caspase 3).

Conclusions

  • DHA exhibits protective effects against UC by mitigating oxidative stress and inflammation.
  • DHA influences apoptotic and necroptotic pathways, suggesting a novel therapeutic mechanism.
  • DHA represents a promising therapeutic candidate for managing ulcerative colitis.