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甲基丁香酚对大鼠脊髓损伤模型所致胃损伤影响的研究

Study of the Effect of Methyl Eugenol on Gastric Damage Produced by Spinal Cord Injury Model in the Rat.

作者信息

Cruz-Antonio Leticia, Sánchez-Mendoza María Elena, García-Machorro Jazmín, López-Lorenzo Yaraset, Arrieta Jesús

机构信息

Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México (UNAM), Av. Guelatao No. 66, Colonia Ejército de Oriente, Iztapalapa, Ciudad de México 09230, Mexico.

Laboratorio de Farmacología de Plantas Medicinales Mexicanas, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Casco de Santo Tomás, Miguel Hidalgo, Ciudad de México 11340, Mexico.

出版信息

Molecules. 2024 Dec 29;30(1):86. doi: 10.3390/molecules30010086.

Abstract

Traumatic spinal cord injury (SCI) is a serious medical condition that places patients at high risk of developing gastric ulceration and gastrointestinal bleeding. One preventative strategy involves the use of omeprazole; however, its chronic use is associated with adverse effects, highlighting the need for alternative therapies. This study evaluated the protective effects of methyl eugenol (ME) on gastric mucosal damage in a rat model of SCI. ME was administered orally at doses of 30, 100, and 177 mg/kg in SCI induced at the T9 level, alongside diclofenac or ketorolac (30 mg/kg each). The enzymatic activity of superoxide dismutase, catalase, and glutathione peroxidase was assessed, and the levels of total glutathione and malondialdehyde were determined using biochemical kits. Additionally, stomach histological sections were analyzed. ME exhibited dose-dependent gastroprotective effects, with maximal protection observed at 177 mg/kg in the presence of diclofenac (9.78 ± 2.16 mm) or ketorolac (12.49 ± 2.17 mm). A histological analysis confirmed these findings. In conclusion, methyl eugenol protects the gastric mucosa from SCI-induced damage, with glutathione peroxidase and catalase playing key roles in its mechanism of gastroprotection.

摘要

创伤性脊髓损伤(SCI)是一种严重的病症,会使患者面临发生胃溃疡和胃肠道出血的高风险。一种预防策略涉及使用奥美拉唑;然而,长期使用该药会产生不良反应,这凸显了对替代疗法的需求。本研究评估了甲基丁香酚(ME)对SCI大鼠模型胃黏膜损伤的保护作用。在T9水平诱导SCI的大鼠中,以30、100和177 mg/kg的剂量口服ME,并分别联合双氯芬酸或酮咯酸(各30 mg/kg)。评估了超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的酶活性,并使用生化试剂盒测定了总谷胱甘肽和丙二醛的水平。此外,还对胃组织切片进行了分析。ME表现出剂量依赖性的胃保护作用,在联合双氯芬酸(9.78±2.16 mm)或酮咯酸(12.49±2.17 mm)时,177 mg/kg剂量下观察到最大保护效果。组织学分析证实了这些结果。总之,甲基丁香酚可保护胃黏膜免受SCI诱导的损伤,谷胱甘肽过氧化物酶和过氧化氢酶在其胃保护机制中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d38f/11721453/931de45c22f7/molecules-30-00086-g001.jpg

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