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InformationThe jejunum is delicate because of its nutrient absorptive and immune functions.This study aimed to investigate the potential protective effect of chrysin on methotrexateinduced jejunal toxicity using adult female Wistar rats.This experiment used a total of 24 rats, randomly divided into 6 groups.Group I, served as the normal control and received food and water.Group II, served as a negative control and was induced with methotrexate only (20 mg/kg), Group III received low dose of chrysin (50 mg/kg), Group IV was induced with methotrexate (20 mg/kg) and a low dose of chrysin (50 mg/kg), Group V received a high dose of chrysin (100 mg/kg) and Group VI induced with methotrexate (20 mg/kg) and a high dose of chrysin (100 mg/kg) respectively.At the end of the experiment, jejunal toxicity was measured biochemically and histo-pathologically by light microscopy, and body weight was statistically analyzed using the SPSS version 23 package.Methotrexate elevated serum MDA in the methotrexate only group (1.24 ± 0.71) compared to the control group (1.14 ± 0.32) and reduced antioxidant enzymes (SOD, GSH, CAT), indicating oxidative stress (p < 0.05).Serum TNF-α, IL-1β, IL-6, and PGE-2 levels showed an increase across groups induced with methotrexate, indicating inflammation.Chrysin treatment significantly reduced these biomarkers compared to the control group (p < 0.05).Histological analysis showed methotrexate caused jejunal necrosis, while chrysin alone or with methotrexate preserved normal histoarchitecture.Low and high doses of chrysin improved tissue structure, though high doses alone showed metaplasia.Chrysin is a potential therapeutic agent against methotrexateinduced jejunal toxicity, reducing oxidative damage and inflammation.
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Nwanama et al. (2025) studied this question.
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