Tekirdağ Namık Kemal University, Faculty of Medicine, Department of General Surgery, Tekirdağ, Turkey.
Tekirdağ Namık Kemal University, School of Health, Department of Emergency and Disaster Management, Tekirdağ, Turkey.
Mol Biol Rep. 2020 Nov;47(11):8867-8879. doi: 10.1007/s11033-020-05939-w. Epub 2020 Nov 1.
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.
本研究旨在探讨蜂王浆（RJ）在治疗大鼠乙醇诱导性胃溃疡模型中的应用。将 32 只 Wistar 白化雄性大鼠随机分为 4 组，每组 8 只：I 组 = 对照组，II 组 = 乙醇组，III 组 = RJ+乙醇组，IV 组 = 兰索拉唑+乙醇组。在 II、III 和 IV 组中，动物在禁食 24 小时后经口给予 1ml 无水乙醇以诱导溃疡形成。通过苏木精-伊红（H&E）染色评估胃黏膜的组织病理学变化。免疫组织化学法评估胃组织中诱导型一氧化氮合酶（iNOS）和核因子 kappa β（Nf-κβ）的标记。通过 TUNEL 法测定胃黏膜细胞死亡。通过分光光度法测定氧化状态标志物超氧化物歧化酶（SOD）、丙二醛（MDA）、过氧化氢酶（CAT）和髓过氧化物酶（MPO）的水平。通过实时 PCR 测定胃组织中白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）基因的表达；并测定 TNF-α、IL-10 和 IL-1β水平。结果表明，RJ 可抑制胃黏膜中 iNOS 和 Nf-κβ 的活性，并防止上皮细胞凋亡。特别是与乙醇组相比，RJ+乙醇组中促炎细胞因子 TNF-α和 IL-1β的水平显著降低。此外，MPO 水平的降低表明 RJ 可预防组织损伤，特别是通过预防炎症细胞浸润。该研究表明 RJ 在大鼠乙醇诱导性胃溃疡模型中可能具有胃保护作用。
