Effects of repeated 14-day oral toxicity of fermented Crescentia cujete (L.) on histopathology, GM-CSF, COX-2, antioxidants, and MDA levels in male Sprague Dawley rats.

Authors

Yos Adi Prakoso, Krestel Joy Viernes Isla, Agustina Dwi Wijayanti

Published in

Open veterinary journal. Volume 15. Issue 12. Pages 6527-6540. Epub Dec 31, 2025.

Abstract

Fermented Crescentia cujete L supernatant of fermented Crescentia cujete (SFC) is a potential alternative therapy for ischemic stroke. However, the effects of SFC on various organs, the immune system, antioxidant levels, and malondialdehyde (MDA) still need to be better understood.
This study aimed to analyze the effects of SFC in rat models through a 14-day repeated-dose oral toxicity study, focusing on histopathology, granulocyte-macrophage colony-stimulating factor (GM-CSF) levels, cyclooxygenase-2 (COX-2), antioxidants, and MDA.
This study used 20 male Sprague Dawley rat models. Rats were divided into four groups: 0, 50, 500, and 2,000 mg/kg BW SFC. The therapy was administered orally and repeated once daily for 14 days. On day 15, the rats were euthanized, and samples were collected. The samples were tested against histopathology, enzyme-linked immunosorbent assay, antioxidant level, and MDA. The data were statistically analyzed.
The results indicated that SFC did not affect histopathology (p ≥ 0.05), except for an increase in bronchial associated lymphoid tissue activity in lung tissue and congestion in the stomach mucosa (p ≤ 0.05). SFC did not influence the rats' serum protein levels (p ≥ 0.05), but it did increase the level of GM-CSF and decrease the level of COX-2 in the serum and various organs (p ≤ 0.05). Additionally, SFC increased the activity of catalase, glutathione peroxidase, glutathione, superoxide dismutase, and total antioxidants while decreasing the MDA level at a dosage of 2,000 mg/kg BW (p ≤ 0.05).
The 14-day repeated-dose oral toxicity study of SFC did not show severe histopathological changes; however, it increased GM-CSF and antioxidant levels, which suppressed COX-2 and MDA levels.

PMID:
42376515
Bibliographic data and abstract were imported from PubMed on 30 Jun 2026.

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