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Alleviation of Liver Dysfunction, Oxidative Stress and Inflammation Underlies the Protective Effect of Ferulic Acid in Methotrexate-Induced Hepatotoxicity.
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-05-20 , DOI: 10.2147/dddt.s237107 Mozhdeh Roghani 1 , Heibatullah Kalantari 1, 2 , Mohammad Javad Khodayar 1, 2 , Layasadat Khorsandi 3 , Mojtaba Kalantar 4 , Mehdi Goudarzi 5 , Hadi Kalantar 1, 2
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-05-20 , DOI: 10.2147/dddt.s237107 Mozhdeh Roghani 1 , Heibatullah Kalantari 1, 2 , Mohammad Javad Khodayar 1, 2 , Layasadat Khorsandi 3 , Mojtaba Kalantar 4 , Mehdi Goudarzi 5 , Hadi Kalantar 1, 2
Affiliation
Introduction: In multiple studies, involvement of oxidative stress in the pathogenesis of methotrexate (MTX)-mediated liver damage has been confirmed. Use of many drugs has been examined experimentally in order to prevent or diminish oxidative stress. However, no study has yet examined the effects of ferulic acid (FA) on MTX-induced liver damage. This study aimed at evaluating the effects of FA on protection against liver damage induced by MTX in mice.
Materials and Methods: In this the mice were divided into five groups in a random manner: I) control; II) MTX (20 mg/kg); III and IV) FA (50 and 100 mg/kg) + MTX; and V) FA (100 mg/kg), and we measured serum factors, oxidative stress and inflammatory factors.
Results: In the MTX group, accumulation of inflammatory cells, accumulation of red blood cell (RBC), and nuclear pyknosis (NP) were detected in the liver. In line with the histological data, the levels of nitric oxide (NO), malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-α increased (TNF-α), whereas the reduced glutathione (GSH), catalase (CAT), total antioxidant capacity (TAC), superoxide dismutase (SOD), and glutathione peroxidase (GPx) content reduced in the MTX group. However, FA ameliorated these hazardous effects in the antioxidant and anti-inflammatory systems in MTX-treated groups.
Conclusion: Based on our findings, oxidative stress impairment and MTX-induced liver damage were ameliorated following FA pretreatment at both histological and biochemical levels. Therefore, FA can be effectively used in abrogation of MTX-induced toxicity.
Keywords: methotrexate, oxidative damage, inflammation, ferulic acid, mice
中文翻译：
缓解肝功能障碍、氧化应激和炎症是阿魏酸在甲氨蝶呤诱导的肝毒性中的保护作用的基础。
简介：在多项研究中，已证实氧化应激参与甲氨蝶呤 (MTX) 介导的肝损伤的发病机制。为了预防或减少氧化应激，已经通过实验检查了许多药物的使用。然而，尚未有研究检查阿魏酸 (FA) 对 MTX 诱导的肝损伤的影响。本研究旨在评估 FA 对 MTX 诱导的小鼠肝损伤的保护作用。
材料与方法：本实验将小鼠随机分为五组：I)对照组；二）甲氨蝶呤（20毫克/公斤）；III 和 IV) FA (50 和 100 mg/kg) + MTX；和 V) FA (100 mg/kg)，我们测量了血清因子、氧化应激和炎症因子。
结果：在 MTX 组中，在肝脏中检测到炎症细胞的积累、红细胞 (RBC) 的积累和核固缩 (NP)。与组织学数据一致，一氧化氮 (NO)、丙二醛 (MDA)、白细胞介素 6 (IL-6) 和肿瘤坏死因子-α (TNF-α) 水平升高，而还原型谷胱甘肽 (GSH) 、过氧化氢酶 (CAT)、总抗氧化能力 (TAC)、超氧化物歧化酶 (SOD) 和谷胱甘肽过氧化物酶 (GPx) 的含量在 MTX 组中降低。然而，FA 改善了 MTX 治疗组的抗氧化和抗炎系统中的这些有害作用。
结论：根据我们的研究结果，FA 预处理后的组织学和生化水平均改善了氧化应激损伤和 MTX 诱导的肝损伤。因此，FA 可以有效地用于消除 MTX 诱导的毒性。
关键词：甲氨蝶呤，氧化损伤，炎症，阿魏酸，小鼠
更新日期：2020-05-20
Materials and Methods: In this the mice were divided into five groups in a random manner: I) control; II) MTX (20 mg/kg); III and IV) FA (50 and 100 mg/kg) + MTX; and V) FA (100 mg/kg), and we measured serum factors, oxidative stress and inflammatory factors.
Results: In the MTX group, accumulation of inflammatory cells, accumulation of red blood cell (RBC), and nuclear pyknosis (NP) were detected in the liver. In line with the histological data, the levels of nitric oxide (NO), malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-α increased (TNF-α), whereas the reduced glutathione (GSH), catalase (CAT), total antioxidant capacity (TAC), superoxide dismutase (SOD), and glutathione peroxidase (GPx) content reduced in the MTX group. However, FA ameliorated these hazardous effects in the antioxidant and anti-inflammatory systems in MTX-treated groups.
Conclusion: Based on our findings, oxidative stress impairment and MTX-induced liver damage were ameliorated following FA pretreatment at both histological and biochemical levels. Therefore, FA can be effectively used in abrogation of MTX-induced toxicity.
Keywords: methotrexate, oxidative damage, inflammation, ferulic acid, mice
中文翻译：
缓解肝功能障碍、氧化应激和炎症是阿魏酸在甲氨蝶呤诱导的肝毒性中的保护作用的基础。
简介：在多项研究中，已证实氧化应激参与甲氨蝶呤 (MTX) 介导的肝损伤的发病机制。为了预防或减少氧化应激，已经通过实验检查了许多药物的使用。然而，尚未有研究检查阿魏酸 (FA) 对 MTX 诱导的肝损伤的影响。本研究旨在评估 FA 对 MTX 诱导的小鼠肝损伤的保护作用。
材料与方法：本实验将小鼠随机分为五组：I)对照组；二）甲氨蝶呤（20毫克/公斤）；III 和 IV) FA (50 和 100 mg/kg) + MTX；和 V) FA (100 mg/kg)，我们测量了血清因子、氧化应激和炎症因子。
结果：在 MTX 组中，在肝脏中检测到炎症细胞的积累、红细胞 (RBC) 的积累和核固缩 (NP)。与组织学数据一致，一氧化氮 (NO)、丙二醛 (MDA)、白细胞介素 6 (IL-6) 和肿瘤坏死因子-α (TNF-α) 水平升高，而还原型谷胱甘肽 (GSH) 、过氧化氢酶 (CAT)、总抗氧化能力 (TAC)、超氧化物歧化酶 (SOD) 和谷胱甘肽过氧化物酶 (GPx) 的含量在 MTX 组中降低。然而，FA 改善了 MTX 治疗组的抗氧化和抗炎系统中的这些有害作用。
结论：根据我们的研究结果，FA 预处理后的组织学和生化水平均改善了氧化应激损伤和 MTX 诱导的肝损伤。因此，FA 可以有效地用于消除 MTX 诱导的毒性。
关键词：甲氨蝶呤，氧化损伤，炎症，阿魏酸，小鼠
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