Akdemir Fazile Nur Ekinci, Güler Mustafa Can, Eraslan Ersen, Tanyeli Ayhan, Yildirim Serkan
Department of Nutrition and Dietetics, Faculty of Health Science, Ağrı İbrahim Çeçen University, Ağrı, Turkey.
Department of Physiology, Faculty of Medicine, Atatürk University, 25240, Erzurum, Turkey.
Naunyn Schmiedebergs Arch Pharmacol. 2024 Dec 24. doi: 10.1007/s00210-024-03733-0.
This study evaluates the protective effects of sinapic acid (SA), a polyphenolic compound with diverse biological activities, against ethanol-induced gastric ulcers in rats. A gastric ulcer model was established using ethanol (ETH), and the experimental groups received either omeprazole (OMEP, 20 mg/kg) or SA at doses of 20 mg/kg and 40 mg/kg via oral gavage for 14 days. Biochemical markers, including total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), malondialdehyde (MDA), and myeloperoxidase (MPO) activity, were assessed alongside proinflammatory cytokines (tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and IL-6) using ELISA. Histopathological and immunohistochemical analyses were conducted to evaluate tissue integrity and apoptosis. Statistical analysis was performed using one-way ANOVA, followed by Tukey's HSD test for post hoc comparisons. For non-parametric data, the Kruskal-Wallis test and Mann-Whitney U test were used. A p-value < 0.05 was considered statistically significant. Results revealed that SA significantly enhanced antioxidant defenses, as evidenced by elevated TAS levels and reductions in TOS, OSI, MPO activity, and MDA levels (p < 0.05). Additionally, SA treatment mitigated inflammation and apoptosis by decreasing TNF-α, IL-1β, IL-6, and Bax expression (p < 0.05). These effects were comparable to those observed with OMEP, a widely used clinical agent. Notably, the findings underscore SA's potential as a novel therapeutic agent for managing ethanol-induced gastric ulcers. By targeting oxidative stress and inflammatory pathways, SA could complement or serve as an alternative to current treatment strategies. Future research should focus on exploring SA's molecular mechanisms, dose optimization, and long-term efficacy in clinical settings, paving the way for its integration into therapeutic regimens for gastric mucosal injuries.
本研究评估了芥子酸(SA)这种具有多种生物活性的多酚化合物对大鼠乙醇诱导型胃溃疡的保护作用。使用乙醇(ETH)建立胃溃疡模型,实验组通过口服灌胃给予奥美拉唑(OMEP,20 mg/kg)或20 mg/kg和40 mg/kg剂量的SA,持续14天。使用酶联免疫吸附测定法(ELISA)评估包括总抗氧化状态(TAS)、总氧化剂状态(TOS)、氧化应激指数(OSI)、丙二醛(MDA)和髓过氧化物酶(MPO)活性在内的生化标志物以及促炎细胞因子(肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和IL-6)。进行组织病理学和免疫组织化学分析以评估组织完整性和细胞凋亡。使用单因素方差分析进行统计分析,随后使用Tukey's HSD检验进行事后比较。对于非参数数据,使用Kruskal-Wallis检验和Mann-Whitney U检验。p值<0.05被认为具有统计学意义。结果显示,SA显著增强了抗氧化防御能力,表现为TAS水平升高以及TOS、OSI、MPO活性和MDA水平降低(p<0.05)。此外,SA治疗通过降低TNF-α、IL-1β、IL-6和Bax表达减轻了炎症和细胞凋亡(p<0.05)。这些作用与广泛使用的临床药物OMEP所观察到的作用相当。值得注意的是,这些发现强调了SA作为治疗乙醇诱导型胃溃疡的新型治疗剂的潜力。通过靶向氧化应激和炎症途径,SA可以补充或替代当前的治疗策略。未来的研究应专注于探索SA的分子机制、剂量优化以及在临床环境中的长期疗效,为将其纳入胃黏膜损伤治疗方案铺平道路。