Royal jelly attenuates gastric mucosal injury in a rat ethanol-induced gastric injury model
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ORIGINAL ARTICLE
Royal jelly attenuates gastric mucosal injury in a rat ethanol-induced gastric injury model Yasin Duran1 · İhsan Karaboğa2 · Fatin Rüştü Polat1 · Elif Polat3 · Zeynep Fidanol Erboğa3 · Mehmet Akif Ovalı4 · Rahime Özlem Öztopuz5 · Aliye Çelikkol6 · Ahsen Yılmaz6 Received: 15 May 2020 / Accepted: 20 October 2020 © Springer Nature B.V. 2020
Abstract 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. Keywords Royal Jelly · Gastric ulcer · Inducible nitric oxide synthase · Nuclear factor-kappa beta · Apoptosis
Introduction
* İhsan Karaboğa [email protected]; [email protected] 1
Tekirdağ Namık Kemal University, Faculty of Medicine, Department of General Surgery, Tekirdağ, Turkey
2
Tekirdağ Namık Kemal University, School of Health, Department of Emergency and Disaster Management, Tekirdağ, Turkey
3
Tekirdağ Namık Kemal University, Faculty of Medicine, Department of Histology and Embryology, Tekirdağ, Turkey
4
Çanakkale Onsekiz Mart University, Faculty of Medicine, Department of Physiology, Çanakkale, Turkey
5
Çanakkale Onsekiz Mart University, Faculty of Medicine, Department of Biophysics, Çanakkale, Turkey
6
Tekirdağ Namık Kemal University, Faculty of Medicine, Department of Medical Biochemistry, Tekirdağ, Turkey
Gastric ulcers, characterized by ulceration of the gastric mucosa, inflammatory cell infiltration, and necrosis, affect approximately 10% of the world population [1, 2]. Although the etiology of gastric ulcers has yet
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