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提取物可预防甲氨蝶呤诱导的肝毒性：一种计算和药理学方法。

Extract Protects against Methotrexate-Induced Hepatotoxicity: A Computational and Pharmacological Approach.

机构信息

College of Natural and Health Sciences, Zayed University, Abu Dhabi 00000, UAE.

Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.

出版信息

Molecules. 2020 May 29;25(11):2540. doi: 10.3390/molecules25112540.

DOI:10.3390/molecules25112540
PMID:32486047
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7321289/
Abstract

extract possess several promising biological activities; currently, it is clinically employed in the management of several diseases. This research work aimed to extrapolate the antioxidant and anti-inflammatory effects of (Gb) in methotrexate (MTX)-induced liver toxicity model. These effects were analyzed using different in vivo experimental approaches and by bioinformatics analysis. Male SD rats were grouped as follows: saline; MTX; Gb (pretreated for seven days with 60, 120, and 180 mg/kg daily dose before MTX treatment); silymarin (followed by MTX treatment); Gb 180 mg/kg daily only; and silymarin only. Histopathological results revealed that MTX induced marked hepatic injury, associated with a substantial surge in various hepatic enzymes such as alanine transaminase (ALT), aspartate transaminase (AST), and serum alkaline phosphatase (ALP). Furthermore, MTX caused the triggering of oxidative distress associated with a depressed antioxidant system. All these injury markers contributed to a significant release of apoptotic (caspase-3 and c-Jun N-terminal kinases (JNK)) and tumor necrosis factor (TNF-α)-like inflammatory mediators. Treatment with Gb counteracts MTX-mediated apoptosis and inflammation dose-dependently along with modulating the innate antioxidative mechanisms such as glutathione (GSH) and glutathione S-transferase (GST). These results were further supplemented by in silico study to analyze drug-receptor interactions (for several Gb constituents and target proteins) stabilized by a low energy value and with a good number of hydrogen bonds. These findings demonstrated that Gb could ameliorate MTX-induced elevated liver reactive oxygen species (ROS) and inflammation, possibly by JNK and TNF-α modulation

摘要

（Gb）具有多种有前途的生物活性；目前，它在多种疾病的治疗中得到临床应用。本研究旨在推断（Gb）在甲氨蝶呤（MTX）诱导的肝毒性模型中的抗氧化和抗炎作用。这些作用通过不同的体内实验方法和生物信息学分析进行了分析。雄性 SD 大鼠分为以下几组：生理盐水；MTX；Gb（在 MTX 处理前用 60、120 和 180mg/kg 每日剂量预处理七天）；水飞蓟素（继 MTX 处理后）；Gb 180mg/kg 每日仅；和水飞蓟素仅。组织病理学结果表明，MTX 诱导了明显的肝损伤，与各种肝酶如丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）和血清碱性磷酸酶（ALP）的大量激增有关。此外，MTX 引起了与抗氧化系统抑制相关的氧化应激触发。所有这些损伤标志物导致凋亡（caspase-3 和 c-Jun N-末端激酶（JNK））和肿瘤坏死因子（TNF-α）样炎症介质的显著释放。Gb 治疗以剂量依赖性方式拮抗 MTX 介导的凋亡和炎症，同时调节内源性抗氧化机制，如谷胱甘肽（GSH）和谷胱甘肽 S-转移酶（GST）。这些结果通过计算机模拟研究进一步得到补充，该研究分析了药物-受体相互作用（针对几种 Gb 成分和靶蛋白），这些相互作用由低能量值和大量氢键稳定。这些发现表明，Gb 可以改善 MTX 诱导的升高的肝脏活性氧（ROS）和炎症，可能通过 JNK 和 TNF-α 调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/691f746176ec/molecules-25-02540-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/4a11e7a1a98b/molecules-25-02540-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/005b1ffbca12/molecules-25-02540-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/50ec3ffc60ed/molecules-25-02540-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/f851c6ee01d3/molecules-25-02540-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/b416d4554aaa/molecules-25-02540-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/3e6fcc722e32/molecules-25-02540-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/bc386f94e6e7/molecules-25-02540-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/326e5ffd472e/molecules-25-02540-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/84f2696cd904/molecules-25-02540-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/5b6f9be5859d/molecules-25-02540-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/691f746176ec/molecules-25-02540-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/4a11e7a1a98b/molecules-25-02540-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/005b1ffbca12/molecules-25-02540-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/50ec3ffc60ed/molecules-25-02540-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/f851c6ee01d3/molecules-25-02540-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/b416d4554aaa/molecules-25-02540-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/3e6fcc722e32/molecules-25-02540-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/bc386f94e6e7/molecules-25-02540-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/326e5ffd472e/molecules-25-02540-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/84f2696cd904/molecules-25-02540-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/5b6f9be5859d/molecules-25-02540-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2299/7321289/691f746176ec/molecules-25-02540-g008.jpg

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