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通过质和亡通路,L-卡尼丁减轻甲甲酸诱导的皮质神经毒性

Kemal Çavdarlı¹, Zafer Usta², Özlem Türkoglu³

¹ProDentalia Dental Clinic, Konyaaltı/Antalya, Turkey.

Journal of applied toxicology : JAT

|October 29, 2025

概括

利卡尼丁 (LCR) 有效地保护大鼠大脑皮层免受甲醇 (MTX) 诱导的神经毒性. 这项研究表明,LCR可以减少MTX诱导的损伤,质激活和亡,突出显示其神经保护潜力.

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 (MTX) 是一种重要的化疗和免疫抑制剂.
它的使用受限于剂量依赖的神经毒性,特别是在大脑皮层.
MTX神经毒性涉及氧化应激,线粒体问题,质激活和亡.

研究的目的:

在大鼠模型中研究L-卡尼丁 (LCR) 对MTX诱导的皮质损伤的神经保护作用.
评估LCR对神经毒性的组织学和分子标记物的影响.

主要方法:

24只Wistar大鼠被分为对照组,MTX,LCR和MTX+LCR组.
每天给药MTX (20 mg/kg),每天给药LCR (200 mg/kg) 持续10天.
皮质组织被分析使用组织病理学,免疫组织化学 (GFAP,OLIG2) 和qRT-PCR (BAX,BCL2).

主要成果:

MTX诱导了严重的皮质退行,,反应性星病和寡质细胞激活.
MTX显著增加了BAX/BCL2亡比率.
同时治疗LCR减少了组织学损伤,减弱了质激活,并将亡平衡转向细胞存活.

结论:

在老鼠中,L-卡尼丁显示出对MTX诱导的皮质损伤具有显著的神经保护功效.
LCR可以减轻MTX对皮质组织,质细胞和亡的有害影响.
LCR是管理MTX神经毒性的有前途的治疗药物.

关键词:

在BAX/BCL2中.对于L-卡尼丁来说,它是一种灭症 (apoptosis) 是一种死亡的过程.大脑皮层大脑皮层状腺激活的激活方式甲基特雷克萨酸盐的使用方法神经保护性神经保护剂神经毒性的作用.氧化应激是一种氧化应激.

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