Selmi Slimen, Rtibi Kais, Grami Dhekra, Sebai Hichem, Marzouki Lamjed
Higher Institute of Biotechnology of Beja, Laboratory Functional Physiology and Bio-resources Valorisation, University of Jendouba, Avenue Habib Bourguiba, BP, 382, 9000, Beja, Tunisia.
Lipids Health Dis. 2017 Aug 14;16(1):152. doi: 10.1186/s12944-017-0546-y.
Massive alcohol drinking can lead to gastric ulcer. In the present study we investigated the gastroprotective effect of Citrus sinensis peel aqueous extract (CSPE) and Hesperidin (H) in ethanol (EtOH) induced oxidative stress and peptic ulcer in rats.
Seventy adult male Wistar rats were divided into seven groups of 10 each: control, EtOH (4 g/kg b.w.), EtOH + various doses of CSPE (100, 200 and 400 mg/kg, b.w.), EtOH + Hesperidin (50 mg/kg, p.o.) and EtOH + Omeprazole (OM, 20 mg/kg, p.o.). Animals were perorally (p.o.) pre-treated with CSPE during 15 days and intoxicated with a single oral administration of EtOH (4 g/kg b.w.) during 2 h. Gastric ulcer was induced in rats with a single dose of ethanol (EtOH). Ulcer index, gene expression of gastric cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), malondialdhyde (MDA), hydrogen peroxide HO and Thiol groups (-SH) content in stomach and antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and gluthation peroxidise (GPx) were measured. Furthermore, histopathological examinations were performed.
The results showed that ethanol induced gastric damage, improving oxidative stress markers level such as MDA (121 ± 4.45 nmol/mg proteins) and HO (24.62 ± 1.04 μmol/mg proteins), increased pro-inflammatory cytokine (TNF-α level), as well as the expression of COX-2 in the ethanol group. However, a significant depletion of enzymatic and non-enzymatic antioxidants were observed, such as, GPx (72%), SOD (57.5%), CAT (41.6%) and -SH (50%). The lesions were associated with severe histopathological damage. The both Citrus sinensis peel aqueous extract (CSPE) and hesperidin significantly protect against all gastric damages caused by ethanol administration in rats.
We propose that CSPE and hesperidin exhibit protective effects in EtOH-induced peptic ulcer in rat. This protection might be related in to part its antioxidant properties as well as its opposite effects on some studied intracellular mediators.
大量饮酒会导致胃溃疡。在本研究中，我们调查了橙子皮水提取物（CSPE）和橙皮苷（H）对乙醇（EtOH）诱导的大鼠氧化应激和消化性溃疡的胃保护作用。
将70只成年雄性Wistar大鼠分为7组，每组10只：对照组、乙醇组（4 g/kg体重）、乙醇 + 不同剂量CSPE组（100、200和400 mg/kg体重）、乙醇 + 橙皮苷组（50 mg/kg，口服）和乙醇 + 奥美拉唑组（OM，20 mg/kg，口服）。动物连续15天经口（口服）给予CSPE预处理，然后在2小时内单次口服乙醇（4 g/kg体重）使其中毒。用单剂量乙醇（EtOH）诱导大鼠胃溃疡。测量溃疡指数、胃环氧化酶-2（COX-2）、肿瘤坏死因子α（TNF-α）、丙二醛（MDA）、过氧化氢（HO）和巯基（-SH）在胃中的含量以及抗氧化酶超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）。此外，进行了组织病理学检查。
结果表明，乙醇诱导胃损伤，使氧化应激标志物水平如MDA（121±4.45 nmol/mg蛋白质）和HO（24.62±1.04 μmol/mg蛋白质）升高，促炎细胞因子（TNF-α水平）增加，以及乙醇组中COX-2的表达增加。然而，观察到酶促和非酶促抗氧化剂显著消耗，如GPx（72%）、SOD（57.5%）、CAT（41.6%）和-SH（50%）。这些损伤与严重的组织病理学损伤相关。橙子皮水提取物（CSPE）和橙皮苷均能显著保护大鼠免受乙醇给药引起的所有胃损伤。
我们提出CSPE和橙皮苷对乙醇诱导的大鼠消化性溃疡具有保护作用。这种保护作用可能部分与其抗氧化特性以及对一些研究的细胞内介质的相反作用有关。
