Gastroprotective and ulcer healing potentials of Nigerian Bee Propolis flavonoid extract on acetic acid-induced gastric ulcers in albino rats (Wistar Strains)

Oyetayo, Noah Segun; Kodie, Dorcas Oyueley; Nwakasi, Martins I.; Afolabi, Oladapo O.; Jarikre, Theophilus Aghogho; Eyarefe, Oghenemega David; Emikpe, Benjamin Obukowho

doi:10.1007/s13596-022-00674-y

Cited by 2 publications

(1 citation statement)

References 39 publications

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“…PUD results from an imbalance between the protective (e.g., mucus, bicarbonate, prostaglandins, antioxidant system and cell proliferation) and destructive (e.g., gastric acid, pepsin, Helicobacter pylori , stress, nonsteroidal anti-inflammatory drugs (NSAIDs) and alcohol) factors (Laine et al 2008 ; Sverdén et al 2019 ), while impaired gastric blood flow, oxidant damage, apoptosis, production of reactive oxygen metabolites and pro-inflammatory cytokines (e.g., tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β) along with alterations in the expressions of nuclear factor kappa B (NF-κB) and prostaglandins (PGI2 and PGE2) aggravate gastric injury (Arabaci Tamer et al 2021 ; Kolgazi et al 2017 ; Tamer et al 2022 ). Experimental gastric ulcer induced by acetic acid, which affects the entire gastric mucosa and submucosa and penetrates the muscularis mucosa, mimics the morphological and clinical findings observed in peptic ulcer patients (Arabacı Tamer et al 2020 ; Okabe and Magase 2005 ), and therefore it is widely used as a chronic gastric ulcer model to investigate putative anti-ulcer alternative medications (Oyetayo et al 2022 ; Wang et al 2022 ).…”

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confidence: 99%

Neuropeptide W facilitates chronic gastric ulcer healing by the regulation of cyclooxygenase and NF-κB signaling pathways

Arabacı Tamer,

Mermer,

Erdoğan

et al. 2024

Inflammopharmacol

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Aims Putative beneficial effects of neuropeptide W (NPW) in the early phase of gastric ulcer healing process and the involvement of cyclooxygenase (COX) enzymes were investigated in an acetic acid-induced gastric ulcer model. Main methods In anesthetized male Sprague–Dawley rats, acetic acid was applied surgically on the serosa and then a COX-inhibitor (COX-2-selective NS-398, COX-1-selective ketorolac, or non-selective indomethacin; 2 mg/kg/day, 3 mg/kg/day or 5 mg/kg/day; respectively) or saline was injected intraperitoneally. One h after ulcer induction, omeprazole (20 mg/kg/day), NPW (0.1 μg/kg/day) or saline was intraperitoneally administered. Injections of NPW, COX-inhibitors, omeprazole or saline were continued for the following 2 days until rats were decapitated at the end of the third day. Key findings NPW treatment depressed gastric prostaglandin (PG) I2 level, but not PGE2 level. Similar to omeprazole, NPW treatment significantly reduced gastric and serum tumor necrosis factor-alpha and interleukin-1 beta levels and depressed the upregulation of nuclear factor kappa B (NF-κB) and COX-2 expressions due to ulcer. In parallel with the histopathological findings, treatment with NPW suppressed ulcer-induced increases in myeloperoxidase activity and malondialdehyde level and replenished glutathione level. However, the inhibitory effect of NPW on myeloperoxidase activity and NPW-induced increase in glutathione were not observed in the presence of COX-1 inhibitor ketorolac or the non-selective COX-inhibitor indomethacin. Significance In conclusion, NPW facilitated the healing of gastric injury in rats via the inhibition of pro-inflammatory cytokine production, oxidative stress and neutrophil infiltration as well as the downregulation of COX-2 protein and NF-κB gene expressions.

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