氧化应激和炎症在饮酒引起的胃溃疡发展中起着关键作用。源自膳食的微量元素硼酸显示出强大的抗氧化和抗炎功能。然而，硼酸的具体机制尚不清楚，其在防止胃损伤方面的有效性也未知。因此，本研究旨在评估硼酸在酒精诱导的胃溃疡中的保护作用，并阐明其潜在机制。在大鼠中通过75%口服乙醇诱导胃溃疡，并通过组织病理学检查、ELISA检测和qRT-PCR评估预防性硼酸治疗（浓度为100mg/kg）的有效性。病理学评估显示硼酸减轻了胃黏膜损伤。硼酸降低了反应性氧化物种(ROS)和丙二醛(MDA)的浓度以及整体氧化状态，同时改善了抗氧化状态。它降低了肿瘤坏死因子-alpha (TNF-α)和白细胞介素-6 (IL-6)的浓度。硼酸预处理降低了JAK2和STAT3的mRNA表达，而增加了AMPK的表达。此外，硼酸预处理还提高了Sema3A和PlexinA1的水平，降低了同型半胱氨酸的水平。我们的结果表明，硼酸通过调节氧化和炎症反应，保护胃黏膜免受乙醇损伤。此外，我们的发现还暗示，硼酸的胃保护活性可以归因于其在AMPK调控的IL-6/JAK2/STAT3信号通路中的调节功能，而Sema3A/PlxnA1轴和同型半胱氨酸可能参与了这一过程。©2023年作者授权给施普林格科学商业传媒有限责任公司，施普林格自然出版集团的一部分。

Oxidative stress and inflammation have pivotal roles in gastric ulcer development caused by alcohol consumption. Trace element boric acid taken into the human and animal body from dietary sources displays strong antioxidant and anti-inflammatory functions. However, the mechanisms underlying these actions of boric acid remain unclear, and its effectiveness in preventing gastric lesions is unknown. Therefore, the present study was undertaken to evaluate the protective effects of boric acid in alcohol-induced gastric ulcer and elucidate its potential mechanisms. Gastric ulcer was induced by 75% oral ethanol administration in rats, and the effectiveness of prophylactic boric acid treatment at 100 mg/kg concentration was assessed by histopathological examination, ELISA assay and qRT-PCR. Gross macroscopic and histopathological evaluations revealed that boric acid alleviated gastric mucosal lesions. Boric acid decreased reactive oxygen species (ROS) and malondialdehyde (MDA) concentration and the overall oxidation state of the body while improving antioxidant status. It reduced the concentration of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The mRNA expression of JAK2 and STAT3 was decreased while the expression of AMPK was increased with boric acid pretreatment. Moreover, Sema3A and PlexinA1 levels were elevated upon boric acid pretreatment, and homocysteine levels were reduced. Our results demonstrated that boric acid protects gastric mucosa from ethanol-induced damage by regulating oxidative and inflammatory responses. In addition, our findings suggested that the gastroprotective activity of boric acid could be attributed to its regulatory function in the IL-6/JAK2/STAT3 signaling modulated by AMPK and that Sema3A/PlxnA1 axis and homocysteine are potentially involved in this process.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.