Biochemistry Department, Faculty of Veterinary Medicine, Alexandria University, Alexandria 22758, Egypt.
Biochemistry Department, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, Egypt.
Oxid Med Cell Longev. 2018 Jul 9;2018:6703296. doi: 10.1155/2018/6703296. eCollection 2018.
Gastric ulcers are among the most broadly perceived illnesses affecting individuals. Alcohol consumption is the main cause of gastric ulceration. This study assessed the protective effects of (SP) extract against ethanol-induced gastric ulcer and elucidated the conceivable underlying mechanisms involved. For this purpose, 40 rats were allotted into 4 equal groups (control, ethanol- (EtOH-) treated, and SP-treated "SP200 and SP400" groups). The control and EtOH-treated groups were given phosphate buffer saline (PBS), and both the SP200 and SP400 groups were given SP extract dissolved in PBS at doses of 200 and 400 mg/kg b.w., respectively. All treatments were given orally for 7 constitutive days. On the 8th day, all rats were fasted for 24 h followed by oral gavage of PBS in the control group and chilled absolute ethanol solution (5 ml/kg b.w.) in the EtOH- and SP-treated groups to induce gastric lesions. One hour later, the rats were sacrificed and the stomachs were harvested. Gross and microscopic examinations of the EtOH-treated group showed severe gastric hemorrhagic necrosis, submucosal edema, destruction of epithelial cells, and reduced glycoprotein content at the mucus surface. These pathological lesions were defeated by SP extract treatment. Administration of SP extract modulated the oxidative stress and augmented the antioxidant defenses. The elevated ethanol-expressed tumor necrosis factor- (TNF-) and interleukin-1 (IL-1) genes, as well as bcl-2-like protein 4 (Bax) and inducible nitric oxide synthase (iNOS), were diminished in the SP-treated group. Curiously, SP extract upregulated endothelial nitric oxide synthase (eNOS) and transforming growth factor-1 (TGF-1) gene expression comparable to that of the EtOH-treated rats. Aggregately, SP exerted antiulcer activities in ethanol-induced gastric ulcer rat models via modulation of oxidant/antioxidant status, mitigation of proinflammatory cytokines, and apoptosis, as well as remodeling of both NOS isoforms.
胃溃疡是最广泛认知的影响个体的疾病之一。饮酒是导致胃溃疡的主要原因。本研究评估了 (SP) 提取物对乙醇诱导的胃溃疡的保护作用，并阐明了可能涉及的潜在机制。为此，将 40 只大鼠分为 4 个相等的组（对照组、乙醇处理组和 SP 处理组“SP200 和 SP400”组）。对照组和乙醇处理组给予磷酸盐缓冲盐水（PBS），SP200 和 SP400 组分别给予溶解在 PBS 中的 SP 提取物，剂量为 200 和 400mg/kg bw。所有治疗均连续 7 天口服给予。第 8 天，所有大鼠禁食 24 小时，然后对照组口服 PBS，乙醇处理组和 SP 处理组口服冷的绝对乙醇溶液（5ml/kg bw），以诱导胃损伤。1 小时后，处死大鼠，取出胃。乙醇处理组的大体和显微镜检查显示严重的胃出血性坏死、黏膜下水肿、上皮细胞破坏和黏液表面糖蛋白含量减少。这些病理损伤被 SP 提取物治疗所克服。SP 提取物的给药调节了氧化应激并增强了抗氧化防御。乙醇表达的肿瘤坏死因子-（TNF-）和白细胞介素-1（IL-1）基因以及 bcl-2 样蛋白 4（Bax）和诱导型一氧化氮合酶（iNOS）在 SP 处理组中降低。有趣的是，SP 提取物上调了内皮型一氧化氮合酶（eNOS）和转化生长因子-1（TGF-1）基因的表达，与乙醇处理组相当。总之，SP 通过调节氧化应激/抗氧化状态、减轻促炎细胞因子和细胞凋亡以及重塑两种 NOS 同工酶，在乙醇诱导的胃溃疡大鼠模型中发挥抗溃疡作用。
