Effects of magnolol on the liver antioxidant status in rats with diabetes.

IF 3.6 3区医学 Q2 PHARMACOLOGY & PHARMACY

Pharmacological Reports Pub Date : 2025-06-01 Epub Date: 2025-03-24 DOI:10.1007/s43440-025-00718-5

Sławomir Dudek, Weronika Borymska, Maria Zych, Dżesika Chełminiak, Magdalena Kimsa-Dudek, Ilona Kaczmarczyk-Żebrowska

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Abstract

Background: Magnolol isolated from Magnolia (Magnolia sp.) flowers are used to support the treatment of diabetes. The aim of this study was to investigate the effects of magnolol on the liver antioxidant status in rats with type 2 diabetes and assess oxidative stress parameters at both biochemical and molecular levels.

Methods: Mature male Wistar rats with high-fat diet (HFD) and streptozotocin (STZ)-induced type 2 diabetes were administered magnolol at doses of 5 or 25 mg/kg body weight po for 4 weeks. Then, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), the concentrations of advanced protein oxidation products (AOPPs) and malondialdehyde (MDA), the total antioxidant response (TAR), and the total oxidative status (TOS) were assessed using commercially available colorimetric kits according to the manufacturers' protocols. The mRNA levels of the cytochrome P450 family 1 subfamily A member 2 (CYP1A2), cytochrome P450 family 2 subfamily E member 1 (CYP2E1), nuclear factor erythroid 2-related factor 2 (NFE2L2), and Kelch like ECH-associated protein 1 (KEAP1) genes were determined using real-time quantitative reverse transcription-polymerase chain reaction (RT‒qPCR). All parameters were analyzed in liver samples.

Results: Compared with 5 mg/kg magnolol, 25 mg/kg magnolol had a more beneficial effect on several indicators of oxidative stress in the liver observed as significant decreases in the activity of SOD and CAT, as well as decreased MDA concentrations. Further, significant increases in the concentrations of AOPPs and native thiols were observed. The gene encoding CYP2E1 was upregulated in diabetic rats compared with control rats. Moreover, compared with diabetic rats, diabetic rats treated with 25 mg/kg magnolol presented increased expression of the KEAP1 gene.

Conclusions: The induction of diabetes is known to disturb redox homeostasis. The administration of magnolol at the higher dose used in this study, might counteract the changes in the liver antioxidant status at both the molecular and biochemical levels. Owing to the positive alterations in some oxidative stress parameters, after further in-depth study, magnolol may be considered a promising compound that could be used to complement diabetes treatment.

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马格诺尔对糖尿病大鼠肝脏抗氧化状态的影响

背景：从白玉兰（Magnolia sp.）花中分离的厚朴酚被用于支持糖尿病的治疗。本研究旨在探讨厚朴酚对2型糖尿病大鼠肝脏抗氧化状态的影响，并在生化和分子水平上评估氧化应激参数。方法：采用高脂饮食（HFD）和链脲佐菌素（STZ）诱导的2型糖尿病成年雄性Wistar大鼠，按5或25 mg/kg体重po给药4周。然后，根据制造商的方案，使用市售比色试剂盒评估超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）的活性、晚期蛋白质氧化产物（AOPPs）和谷胱甘肽过氧化物酶（MDA）的浓度、总抗氧化反应（TAR）和总氧化状态（TOS）。采用实时定量逆转录聚合酶链式反应（RT-qPCR）检测细胞色素P450家族1亚家族A成员2 （CYP1A2）、细胞色素P450家族2亚家族E成员1 （CYP2E1）、核因子红系2相关因子2 （NFE2L2）和Kelch样ech相关蛋白1 （KEAP1）基因的mRNA水平。分析肝脏样本的所有参数。结果：与5 mg/kg厚朴酚相比，25 mg/kg厚朴酚对肝脏氧化应激的几个指标有更有利的影响，SOD和CAT活性显著降低，MDA浓度显著降低。此外，观察到AOPPs和天然硫醇浓度显著增加。与对照大鼠相比，糖尿病大鼠CYP2E1基因表达上调。此外，与糖尿病大鼠相比，25 mg/kg厚朴酚处理的糖尿病大鼠KEAP1基因表达增加。结论：已知糖尿病的诱导会扰乱氧化还原稳态。本研究中使用的高剂量厚朴酚可能在分子和生化水平上抵消肝脏抗氧化状态的变化。由于厚朴酚对某些氧化应激参数的积极改变，经过进一步的深入研究，厚朴酚可能被认为是一种有前景的化合物，可以用于补充糖尿病的治疗。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Pharmacological Reports 医学-药学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

6 months

期刊介绍： Pharmacological Reports publishes articles concerning all aspects of pharmacology, dealing with the action of drugs at a cellular and molecular level, and papers on the relationship between molecular structure and biological activity as well as reports on compounds with well-defined chemical structures. Pharmacological Reports is an open forum to disseminate recent developments in: pharmacology, behavioural brain research, evidence-based complementary biochemical pharmacology, medicinal chemistry and biochemistry, drug discovery, neuro-psychopharmacology and biological psychiatry, neuroscience and neuropharmacology, cellular and molecular neuroscience, molecular biology, cell biology, toxicology. Studies of plant extracts are not suitable for Pharmacological Reports.