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加拿大大麻 (Cannabis sativa) 与特拉马多尔 (tramadol) 和可代因 (codeine) 联合使用对雄性大鼠认知功能的调节作用

Ayokunle Olubode Ademosun¹, Olufunke Florence Ajeigbe², Bodun Oluwaseun Lawrence¹

¹Department of Biochemistry, Federal University of Technology, P.M.B. 704, Akure 340001, Nigeria.

Neurotoxicology

|August 31, 2023

概括

青少年混合可代因,特拉马多尔和大麻会损害大脑的认知能力,并改变神经递质酶活动. 这项研究揭示了这些药物组合的神经毒性机制,影响胆能和纯能系统.

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:

青少年经常结合诸如可代因,特拉马多尔和大麻之类的精神活性物质进行中毒.
这些特定药物组合的神经认知和酶作用在很大程度上仍未得到研究.
了解这些相互作用对于解决潜在的神经毒性和认知障碍至关重要.

研究的目的:

为了评估联合编代因,特拉马多尔和大麻树种对大鼠大脑功能的影响.
阐明与认知,纯能,胆能和抗氧化酶活动相关的神经毒性的潜在机制.

主要方法:

雄性Wistar大鼠被分为八组,接受单剂或联合剂的可代因,特拉马多尔和Cannabis sativa治疗28天.
测量了认知功能,乙胆酶 (AChE),丁胆酶 (BChE),单胺氧化酶 (MAO) 和抗氧化酶活动.
在脑组织中量化了ECTONUCLEOSIDES (NTPdase),ADENOSINE DEAMINASE (ADA) 和MALONDIALDEHYDE的水平.

主要成果:

长期同时服用编解素,特拉马多尔和Cannabis sativa显著抑制了认知功能和关键酶活动 (AChE,BChE,MAO,抗氧化酶).
与对照组相比,在接受治疗的老鼠的大脑中观察到高水平的NTPdase,ADA和malondialdehyde.
鉴定出胆酶酶活性显著降低是导致神经递质中毒的主要机制.

结论:

合并使用的可代因,特拉马多尔和大麻会在老鼠中诱导神经毒性,其特征是认知缺陷和酶配置的改变.
观察到的神经毒性与胆能和纯能信号通路的破坏有关.
这项研究强调了这些药物尾酒对大脑功能的有害影响,并提供了对它们的毒理机制的洞察.

关键词:

大麻sativa是一种大麻.编码因 (Codeine) 是一种蛋白质.认知认知是一种认知.精神活性药物精神活性药物特拉马多尔 (Tramadol) 是一种药物.

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