PDF(Pubmed)
Abstract：
Tobacco and alcohol have been identified as health risk behaviors associated with significant unfavorable health consequences, ranking within the list of the top ten causes of mortality and disability-adjusted life years (DALY). The combustion of tobacco leads to the formation of acrylamide (ACR), which is well known for its neurotoxic effects. Similarly, alcohol consumption has also been widely recognized for its neurotoxic effects. Both substances can affect neurons and neuroglia cells through various pathways. This study sought to examine the impacts of co-administration of ACR and intermittent-access ethanol (IAE) consumption over a period of one month. The experimental group received 20 mg/kg of ACR, administered orally, along with IAE of 20% ethanol sessions lasting 24 h, three times per week. The cognitive outcomes were assessed utilizing the elevated plus maze (EPM), which was employed as a means of assessing the capability to learn and remember, the novel object recognition (NOR) test, which was employed to assess recognition memory, and the Y-maze, which was used to explore a new environment and navigate. Additionally, ELISA assays were performed to examine underlying mechanisms, including markers associated with inflammation (NF-κB, PGE2, and TNF-α), apoptosis (Bcl2, Bax, and Caspase-3), and oxidative stress (MDA, catalase, and GSH). These markers were assessed in the brain homogenate as part of the investigation. Furthermore, a histopathological study was conducted. The findings indicated that NF-κB levels increased significantly in the combination of ACR and IAE groups (ACR + IAE) compared to either the ACR-alone or IAE-alone groups. However, parallel changes were observed in TNF-α, PGE2, Bax, Bcl-2, Caspase-3, GSH, and CAT levels when comparing the ACR + IAE group to the ACR-alone group. Comparable alterations were noted between the ACR + IAE treatment and IAE-alone groups in TNF-α, Bcl-2, MDA, GSH, and CAT levels. Moreover, the histopathological analysis revealed significant changes between the ACR + IAE and the ACR- or IAE-alone groups. Regarding memory parameters assessed using tests including EPM, NOR, and Y-maze, considerable changes were observed across all treatment groups as opposed to the control. Surprisingly, there were no notable differences in the NOR and Y-maze tasks between the alone and combination treatment. Further study is necessary to explore the long-term alteration of co-administering ACR and IAE on behavior, memory, and neurotoxicity-related mechanisms, in order to elucidate their combined effects more clearly.
摘要：
烟草和酒精已被确定为与重大不利健康后果相关的健康危险行为，在十大死亡原因和残疾调整寿命年(DALY)中排名。烟草的燃烧导致丙烯酰胺（ACR）的形成，以其神经毒性作用而闻名。同样，饮酒也因其神经毒性作用而被广泛认可。这两种物质都可以通过各种途径影响神经元和神经胶质细胞。这项研究旨在检查ACR和间歇性获取乙醇（IAE）消耗在一个月的时间内共同施用的影响。实验组服用20mg/kg的ACR，口服给药,伴随着持续24小时的20%乙醇的IAE，每周三次。使用高架迷宫(EPM)评估认知结果，它被用作评估学习和记忆能力的一种手段，新颖的物体识别(NOR)测试，用于评估识别记忆，还有Y迷宫,用于探索新环境和导航。此外,进行ELISA测定以检查潜在的机制，包括与炎症相关的标志物（NF-κB，PGE2和TNF-α)，凋亡(Bcl2，Bax，和Caspase-3），和氧化应激(MDA，过氧化氢酶,和GSH）。作为研究的一部分,在脑匀浆中评估这些标记物。此外，进行了组织病理学研究。研究结果表明,与单独的ACR或单独的IAE组相比,在ACR和IAE组(ACR+IAE)的组合中NF-κB水平显著增加。然而,观察到TNF-α的平行变化，PGE2,Bax,Bcl-2,Caspase-3,GSH,当比较ACR+IAE组与单独ACR组时，CAT水平。在TNF-α中，ACRIAE治疗与IAE单独治疗组之间的变化相当，Bcl-2,MDA,GSH,CAT水平。此外，组织病理学分析显示,ACR+IAE组和ACR-或IAE-单独组之间发生显著变化.关于使用包括EPM在内的测试评估的内存参数，NOR,和Y迷宫，与对照组相比,在所有治疗组中观察到相当大的变化.令人惊讶的是,单独治疗和联合治疗之间的NOR和Y迷宫任务没有显着差异。进一步的研究是必要的，以探讨共同管理ACR和IAE对行为的长期变化，记忆,和神经毒性相关机制，以便更清楚地阐明它们的综合作用。
