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Updated: Sep 4, 2026

Zebrafish Larvae as a Model to Evaluate Potential Radiosensitizers or Protectors
Published on: August 25, 2022
Protective effects of Quercus brantii fruit extract against oxytetracycline-induced intestinal injury in zebrafish
Ghazaleh Kooravand1, Kaveh Rahimi2, Mojtaba Alishahi3
1Department of Basic Sciences, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Abstract:
Zebrafish (Danio rerio) is widely used as a vertebrate model to study intestinal inflammation due to structural and functional similarities of its gastrointestinal tract to mammals. Oxytetracycline (OTC), a commonly used antibiotic in aquaculture, can accumulate in aquatic organisms and disrupt gut homeostasis, inducing oxidative stress and inflammatory responses. This study evaluated the protective effects of hydroalcoholic Quercus brantii fruit extract against OTC-induced intestinal injury in zebrafish larvae. A total of 144 three-day-old larvae were randomly assigned to four experimental groups (n = 36 per group, three replicates of 12 larvae): control (untreated), OTC (10 mg/L for five days), OTC + Quercus brantii fruit extract 10 g/kg diet, and OTC + Quercus brantii fruit extract 20 g/kg diet. Histopathological analysis revealed that OTC exposure caused partial epithelial disruption, reduced mucosal fold height, decreased goblet cell density, and increased infiltration of inflammatory cells. Cotreatment with 10 g/kg Quercus brantii fruit extract partially ameliorated these changes, whereas 20 g/kg significantly preserved epithelial integrity, increased mucosal fold height, and reduced inflammatory cell infiltration. Gene expression analysis showed that OTC significantly upregulated NF-κB, TNF-α, and IL-6 levels. Administration of 10 g/kg Quercus brantii fruit extract reduced NF-κB and TNF-α expression but did not significantly affect IL-6, while 20 g/kg extract significantly decreased all three cytokines. These results indicate that hydroalcoholic Quercus brantii fruit extract exerts protective effects against OTC-induced intestinal injury, likely mediated through NF-κB inhibition.
