Evaluation of Anti-Inflammatory and Antioxidant Effects of Ferulic Acid and Quinic Acid on Acetic Acid-Induced Ulcerative Colitis in Rats

IF 2.8 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Biochemical and Molecular Toxicology Pub Date : 2025-02-17 DOI:10.1002/jbt.70169
Mahsa Ekhtiar, Maryam Ghasemi-Dehnoo, Fatemeh Azadegan-Dehkordi, Nader Bagheri
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Abstract

Ulcerative colitis is a chronic inflammatory disease characterized by oxidative stress and the production of pro-inflammatory cytokines. Ferulic acid and quinic acid, two phenolic compounds, are thought to have potent antioxidant and anti-inflammatory properties. This study aimed to investigate the anti-inflammatory and antioxidant effects of ferulic acid and quinic acid in rats with acetic acid (AA)-induced ulcerative colitis. To this end, 64 Wistar rats were randomly divided into eight groups, each consisting of eight rats. AA was administered intrarectally to induce ulcerative colitis. Ferulic acid (20, 40, and 60 mg/kg), quinic acid (10, 30, 60, and 100 mg/kg), and dexamethasone (2 mg/kg) were received daily for five consecutive days. Then, the macroscopic and histopathological changes in the colon tissue were examined. Finally, the tissue levels of heme oxygenase 1 (HO1), nuclear factor erythroid 2-related factor 2 (NRF2), and NAD(P)H quinone dehydrogenase 1 (NQO1) mRNA expression and pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) were measured using the quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) methods, respectively. AA-induced ulcerative colitis in rats was associated with edema and severe damage to the epithelium, infiltration of inflammatory cells, and the presence of ulcers in the colon tissue. The results showed that rats who were administered AA showed a decrease in the expression of HO-1, Nrf2, and NQO1 and increased protein levels of TNF-α and IL-1β than the control group. Rats were administered ferulic acid, quinic acid and, dexamethasone significantly improved histopathological indices. The expression of HO-1, Nrf2, and NQO1 were upregulated by 60 mg/kg of ferulic acid, 60 and100 mg/kg of quinic acid and, 2 mg/kg of dexamethasone treatment compared to the ulcerative colitis group. The protein levels of TNF-α and IL-1β dose-dependently decreased by ferulic acid and quinic acid treatment compared to the ulcerative colitis group. Ferulic acid and quinic acid effectively reduce inflammation and mucosal damage in rats with ulcerative colitis, especially when administered in high doses. The possible mechanism of anti-inflammatory response by ferulic acid and quinic acid may involve the activating of the Nrf2/HO-1 pathway.

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阿魏酸和奎宁酸对醋酸致溃疡性结肠炎大鼠抗炎和抗氧化作用的评价
溃疡性结肠炎是一种以氧化应激和促炎细胞因子的产生为特征的慢性炎症性疾病。阿魏酸和奎宁酸是两种酚类化合物,被认为具有有效的抗氧化和抗炎特性。本研究旨在探讨阿魏酸和奎宁酸对醋酸(AA)诱导的溃疡性结肠炎大鼠的抗炎和抗氧化作用。为此,将64只Wistar大鼠随机分为8组,每组8只大鼠。直肠内给药AA诱导溃疡性结肠炎。阿魏酸(20、40和60 mg/kg)、奎宁酸(10、30、60和100 mg/kg)和地塞米松(2 mg/kg),连续5天每天服用。然后观察结肠组织的宏观和组织病理学变化。最后,分别采用实时定量聚合酶链式反应(PCR)和酶联免疫吸附法(ELISA)检测各组组织中血红素加氧酶1 (HO1)、核因子2-相关因子2 (NRF2)和NAD(P)H醌脱氢酶1 (NQO1) mRNA表达水平和促炎细胞因子肿瘤坏死因子α (TNF-α)和白细胞介素-1β (IL-1β)水平。aa诱导的大鼠溃疡性结肠炎与水肿、上皮严重损伤、炎症细胞浸润和结肠组织溃疡存在相关。结果显示,AA组大鼠HO-1、Nrf2、NQO1的表达明显低于对照组,TNF-α、IL-1β蛋白水平明显高于对照组。大鼠给予阿魏酸、奎宁酸和地塞米松后,组织病理学指标明显改善。与溃疡性结肠炎组相比,阿魏酸60mg /kg、奎宁酸60mg /kg、100mg /kg和地塞米松2mg /kg组HO-1、Nrf2和NQO1表达上调。与溃疡性结肠炎组相比,阿魏酸和奎宁酸治疗组TNF-α和IL-1β蛋白水平呈剂量依赖性降低。阿魏酸和奎宁酸可有效减轻溃疡性结肠炎大鼠的炎症和粘膜损伤,特别是在大剂量给药时。阿魏酸和奎宁酸抗炎反应的可能机制可能与Nrf2/HO-1通路的激活有关。
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来源期刊
CiteScore
5.80
自引率
2.80%
发文量
277
审稿时长
6-12 weeks
期刊介绍: The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.
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