Scholarly works in Veterinary Surgery and Reproduction

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Author: search.filters.author.Olojo, F. O.

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    Argania spinosa essential oil ameliorates colonic damage and extraintestinal alterations in a rat model of acetic acid‑induced colitis by suppressing oxidative stress and inflammation
    (Springer Nature, 2023) Olojo, F. O.; Akinrinde, A. S.; Ogundairo, S. A.; Ubochi, V. C.
    The present study was designed to elucidate the prophylactic and therapeutic potential of argan oil (AO) (from the kernels of the argan tree, Argania spinosa) against acetic acid (AA)-induced colitis and associated alterations in the liver and kidneys of rats. Colitis was induced by intra-rectal administration of 4% AA solution for 3 consecutive days. Some groups of rats were treated orally with AO (5 mL/kg) for 5 consecutive days before and after AA administration, while other groups were treated with either the vehicle or AO alone. Macroscopic and microscopic lesions in the tissues were assessed, while oxidative stress, antioxidant parameters and myeloperoxidase (MPO) activity were determined by biochemical methods. Haematological and serum chemistry parameters were also evaluated. Administration of AO before or after AA induction produced improvements in body weight gain, faecal consistency, macroscopic and histologic scores of the colonic mucosa compared to rats treated with AA alone. Furthermore, AO treatment caused significant reduction in colonic levels of hydrogen peroxide (H2O2), malondialdehyde (MDA), advanced oxidation protein products (AOPP) and serum MPO activity, while glutathione S-transferase (GST) and superoxide dismutase (SOD) activities were increased in the colon and kidneys, compared to the colitis control. Acetic acid treatment resulted in significant reduction in erythrocyte and leucocyte indices in relation to healthy controls. Taken together, treatment of rats with AO protected colonic tissues from acetic acid-induced inflammation and suggests that the oil may be considered for preventive and therapeutic purposes against inflammatory bowel diseases.
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    Nigella sativa oil protects against cadmium-induced intestinal toxicity via promotion of anti-inflammatory mechanisms, mucin expression and microbiota integrity
    (Mashhad University of Medical Sciences, Iran, 2021) Akinrinde, A. S.; Adekanmbi, A. O.; Olojo, F. O.
    Objective: This study examined the protective effects of Nigella sativa oil (NSO) on cadmium (Cd)-induced alterations affecting gut morphology and microbiota composition, as well as the involvement of mucus glycoprotein (MUC2) and immune-inflammatory markers (TNFα and IL-2) in the colon of rats. Materials and Methods: Male Wistar rats, randomized into four groups, were treated either with distilled water (control), CdCl2 (100 mg/kg), CdCl2+NSO (1 ml/kg) or NSO alone. After the experiments, faecal samples were processed for microbial culture on various selective media, while intestinal segments were prepared for histopathological examination and immunohistochemistry. The composition of NSO was analyzed using Gas Chromatography-Mass Spectrometry (GC-MS). Results: Oral Cd administration provoked dramatic increases in faecal counts of potentially pathogenic bacteria (Staphylococci, Enterococci, Pseudomonas and Escherichia coli), while decreasing probiotic lactobacilli counts. Cadmium treatment caused down-regulation of colonic MUC2 (p=0.003) and IL-2 (p=0.03), but increased TNFα (p=0.034), along with reduced goblet cell counts and mucus production. Conversely, treatment with NSO significantly improved Lactobacilli counts (p=0.042), while reducing the levels of potentially pathogenic species. In addition, NSO significantly restored colonic expressions of MUC2 (p=0.001), TNFα (p=0.007) and IL-2 (p=0.025) to control levels. GC-MS analysis of NSO revealed the presence of the active ingredient, thymoquinone and a high content of unsaturated fatty acids, including trans-13-octadecenoic acid and oleic acid. Conclusion: This study highlights the intestinal mucus, microbiota and immuno-inflammatory system as important protective targets of NSO against Cd-induced intestinal toxicity.