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探索苯甲酸钠对大鼠乙酸诱导的溃疡性结肠炎的治疗潜力。

Exploring the therapeutic potential of sodium benzoate in acetic acid-induced ulcerative colitis in rats.

作者信息

Walia Deepali, Kaur Gurpreet, Jaggi Amteshwar Singh, Bali Anjana

机构信息

Department of Pharmacology, Akal College of Pharmacy and Technical Education, Mastuana Sahib, Sangrur, India.

Department of pharmacognosy, Akal College of Pharmacy and Technical Education, Mastuana Sahib, Sangrur, India.

出版信息

J Basic Clin Physiol Pharmacol. 2019 Aug 30;30(5):jbcpp-2019-0086. doi: 10.1515/jbcpp-2019-0086.

DOI:10.1515/jbcpp-2019-0086
PMID:31469656
Abstract

Background Ulcerative colitis is a chronic mucosal inflammation of the large intestine mainly affecting the colon and rectum. The lack of effective and safe therapeutic agents led to the identification of new therapeutic agents to effectively manage the symptoms and complications of ulcerative colitis. The present study aimed to evaluate the protective effect of sodium benzoate in acetic acid-induced ulcerative colitis in rats. Methods Infusion of 3% acetic acid in the colon through the rectum was done to construct a rat model of ulcerative colitis. After 5 days of infusion, macroscopic, biochemical, and histopathological examinations and disease activity scoring of the colon were done to assess colonic damage. Results Acetic acid infusion resulted in severe inflammation in the colon assessed macroscopically and histopathologically. Moreover, it also led to increase in myeloperoxidase (MPO) and reduction in glutathione (GSH) levels. In the present study, repeated administration of sodium benzoate (400 and 800 mg/kg i.p.) and sulfasalazine (500 mg/kg orally) for 7 days, i.e. 2 days before and continued for 5 days after acetic acid infusion, significantly attenuated macroscopic damage and disease activity score as compared to disease control. Further, it also significantly reduced the levels of MPO and enhanced colonic levels of reduced GSH. However, the lower dose of sodium benzoate (200 mg/kg) did not show sufficient protective effect in acetic acid-induced ulcerative colitis. Further, sodium benzoate per se did not show any effect in normal rats. Conclusions The observed protective effect of sodium benzoate may be due to its antioxidant and anti-inflammatory activities in an ulcerative colitis model.

摘要

背景

溃疡性结肠炎是一种主要影响结肠和直肠的大肠慢性黏膜炎症。缺乏有效且安全的治疗药物促使人们寻找新的治疗药物来有效控制溃疡性结肠炎的症状和并发症。本研究旨在评估苯甲酸钠对乙酸诱导的大鼠溃疡性结肠炎的保护作用。方法:通过直肠向结肠内注入3%的乙酸以构建大鼠溃疡性结肠炎模型。注入5天后,进行宏观、生化和组织病理学检查以及结肠疾病活动评分,以评估结肠损伤情况。结果:从宏观和组织病理学角度评估,乙酸注入导致结肠出现严重炎症。此外,还导致髓过氧化物酶(MPO)水平升高和谷胱甘肽(GSH)水平降低。在本研究中,苯甲酸钠(400和800毫克/千克腹腔注射)和柳氮磺胺吡啶(500毫克/千克口服)连续给药7天,即在乙酸注入前2天开始并在注入后持续5天,与疾病对照组相比,显著减轻了宏观损伤和疾病活动评分。此外,还显著降低了MPO水平并提高了结肠中还原型GSH的水平。然而,较低剂量的苯甲酸钠(200毫克/千克)在乙酸诱导的溃疡性结肠炎中未显示出足够的保护作用。此外,苯甲酸钠本身对正常大鼠没有任何影响。结论:观察到的苯甲酸钠的保护作用可能归因于其在溃疡性结肠炎模型中的抗氧化和抗炎活性。

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