Abstract Title:

Royal jelly attenuates gastric mucosal injury in a rat ethanol-induced gastric injury model.

Abstract Source:

Mol Biol Rep. 2020 Nov ;47(11):8867-8879. Epub 2020 Nov 1. PMID: 33135128

Abstract Author(s):

Yasin Duran, İhsan Karaboğa, Fatin Rüştü Polat, Elif Polat, Zeynep Fidanol Erboğa, Mehmet Akif Ovalı, RahimeÖzlem Öztopuz, Aliye Çelikkol, Ahsen Yılmaz

Article Affiliation:

Yasin Duran


The aim of the study was to investigate traditionally used Royal Jelly (RJ) for treating an ethanol-induced gastric ulcer model in rats. A total of 32 Wistar albino male rats were divided into 4 groups of 8: group I = Control, group II = Ethanol, group III = RJ + Ethanol, and group IV = Lansoprazole + Ethanol. In groups II, III, and IV, animals were administered 1 ml of absolute ethanol orally after a 24-h fast to induce ulcer formation. The histopathological changes in the gastric mucosa were determined using hematoxylin-eosin (H&E) staining. Immunohistochemically, inducible nitric oxide (iNOS) and nuclear factor kappa beta (Nf-κβ) markings were evaluated in gastric tissue. Cell death in the gastric mucosa was determined by the TUNEL method. Oxidative status markers, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), and myeloperoxidase (MPO) levels were determined spectrophotometrically. Expression of the interleukin - 1 beta (IL-1β) and tumor necrosis factor-α (TNF-α) genes in gastric tissues was determined by real-time PCR; and TNF-α, IL-10, and IL-1β levels were determined. RJ was found to inhibit iNOS and Nf-κβ activity in the gastric mucosa and prevent epithelial cell apoptosis. In particular, pro-inflammatory cytokines TNF-α and IL-1β levels were significantly decreased in the RJ + Ethanol group compared to the Ethanol group. In addition, a decrease in the MPO level indicated that RJ prevented tissue damage, especially by preventing inflammatory cell infiltration. The study demonstrated a possible gastroprotective effect of RJ in a rat ethanol-induced gastric ulcer model.

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