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蒙特卢卡斯特可以缓解小鼠中乙胺诱导的肝脑病变

Rehab S Abdelrahman^1,2, Rania R Abdelaziz³, Marwa E Abdelmageed¹

¹Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.

Naunyn-Schmiedeberg's archives of pharmacology

|May 24, 2025

概括

蒙特卢卡斯特通过减少炎症和氧化应激,在大鼠中显示出对肝脑病 (HE) 的显著保护作用. 这种喘药物通过其抗氧化和抗炎机制显示出治疗HE的前景.

科学领域:

肝病学肝病学是一种肝病学.
神经科学是一个神经科学.
药理学药理学是指药理学的学科.

背景情况:

肝脑病 (HE) 是肝病的一种严重的神经精神疾病并发症.
蒙特卢卡斯特 (Mon) 是喘的CysLT1R对手,具有已知的抗氧化和抗炎性质.
蒙特卢卡斯特对HE的治疗潜力仍然未被探索.

研究的目的:

在大鼠模型中研究蒙特卢卡斯特对乙胺诱导的HE的保护作用.
为了阐明蒙特卢卡斯特的潜在肝脏和神经保护机制.

主要方法:

给大鼠注射了硫乙胺 (TAA) 来诱导HE.
蒙特卢卡斯特 (5和10毫克/公斤) 连续7天口服.
评估了肝脏和大脑功能,炎症标志物 (NF-κB,TNF-α),氧化应激 (MDA,NO),PI3K/Akt和caspase-3表达.

主要成果:

蒙特卢卡斯特在TAA诱导的HE大鼠中显著改善了肝脏和大脑功能.
蒙特卢卡斯特抑制了炎症因素,减少了大脑和肝脏中的氧化应激.
蒙特卢卡斯特在大脑中上调PI3K/Akt表达和下调caspase-3表达,从而使组织病理损伤正常化.

结论:

蒙特卢卡斯特在实验性HE模型中表现出显著的肝脏和神经保护作用.
它的机制涉及PI3K/Akt通路的激活,caspase-3的抑制,以及减少炎症和氧化应激标志物.
蒙特卢卡斯特显示出作为肝脏脑病的新型治疗剂的潜力.

关键词:

在Caspase-3中使用.肝脏脑病变肝脏脑病变是一种肝脏脑病变.蒙特利卢卡斯特是一个蒙特利卢卡斯特.在 NF-κBB 中.氧化应激是一种氧化应激.PI3 K/Akt 法律法规酸乙胺的酸乙.

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