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库贝通过CREB/BDNF/Caspase-3信号减轻甲基胺诱导的神经毒性:体内和体内研究

Sattam Khulaif Alenezi¹, Khalid Saad Alharbi¹, Tariq G Alsahli²

¹Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Al Qassim, Saudi Arabia.

Medicina (Kaunas, Lithuania)

|September 27, 2025

概括

库贝通过改善抗氧化剂活性和减少炎症,证明了对甲基胺诱导的认知缺陷的神经保护作用. 这种天然化合物在缓解神经退行和恢复认知功能方面表现有前途.

科学领域:

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.
毒理学毒理学毒理学

背景情况:

甲基胺 (METH) 引起神经毒性和认知障碍.
库贝因其潜在的神经保护性质而受到研究.

研究的目的:

评估库贝宾对METH诱导的神经毒性和认知缺陷的疗效.
评估库贝对氧化应激,炎症和神经递质水平的影响.

主要方法:

给老鼠注射了METH和不同剂量的cubebin.
用莫里斯水迷宫 (MWM) 评估认知功能.
生物化学分析包括神经递质,氧化应激标志物,炎症细胞因子,神经营养因子和亡标志物.

主要成果:

库贝治疗显著改善了MWM任务中的认知表现.
库贝宾调节了氧化应激,减少了炎症标志物,并使神经递质水平正常化.
分子动力学模拟显示了cubebin与关键的神经保护蛋白的相互作用.

结论:

库贝的使用增强了暴露于METH的老鼠的认知功能.
库贝通过减少氧化应激和炎症,表现出神经保护作用.
库贝显示出作为一种治疗药物的潜力,可以对抗METH诱导的神经退行.

关键词:

灭症 (apoptosis) 是一种死亡的过程.在的中.甲基胺的使用方法神经毒性的作用.这些神经递质是神经递质.氧化应激是一种氧化应激.

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相关概念视频

Caspases

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.