Namgyal Dhondup, Ali Sher, Hussain Muhammad Delwar, Kazi Mohsin, Ahmad Ajaz, Sarwat Maryam
Amity Institute of Neuropsychology and Neuroscience, Amity University, Noida 201303, India.
Amity Institute of Pharmacy, Amity University, Noida 201303, India.
Antioxidants (Basel). 2021 Oct 27;10(11):1710. doi: 10.3390/antiox10111710.
Age-related neurodegenerative diseases and vascular dementia are major challenges to the modern health care system. Most neurodegenerative diseases are associated with impaired spatial working memory and anxiety-like behavior. Thus, it is important to understand the underlying cellular mechanisms of neurodegenerative diseases in different regions of the brain to develop an effective therapeutic approach. In our previous research paper, we have reported the ameliorative effect of curcumin in Cd-induced hippocampal neurodegeneration. However, recently many researchers had reported the important role of the prefrontal cortex in higher cognitive functions. Therefore, to look into the cellular mechanism of curcumin protection against Cd-induced prefrontal cortex neurotoxicity, we investigated spatial working memory, anxiety-like behavior and analyzed prefrontal cortex inflammatory markers (IL-6, IL-10, and TNFα), antioxidant enzymes (SOD, GSH, and CAT), and pro-oxidant MDA level. Further, we conducted histological studies of the prefrontal cortex in Swiss albino mice exposed to cadmium (2.5 mg/kg). We observed that curcumin treatment improved the spatial working memory and anxiety-like behavior of mice through reduction of prefrontal cortex neuroinflammation and oxidative stress as well as increasing the number of viable prefrontal cortex neuronal cells. Our result suggests that environmental heavy metal cadmium can induce behavioral impairment in mice through prefrontal cortex cellular inflammation and oxidative stress. We found that curcumin has a potential therapeutic property to mitigate these behavioral and biochemical impairments induced by cadmium.
与年龄相关的神经退行性疾病和血管性痴呆是现代医疗保健系统面临的重大挑战。大多数神经退行性疾病都与空间工作记忆受损和焦虑样行为有关。因此,了解大脑不同区域神经退行性疾病的潜在细胞机制对于开发有效的治疗方法至关重要。在我们之前的研究论文中,我们报道了姜黄素对镉诱导的海马神经退行性变的改善作用。然而,最近许多研究人员报道了前额叶皮质在高级认知功能中的重要作用。因此,为了探究姜黄素对镉诱导的前额叶皮质神经毒性的保护细胞机制,我们研究了空间工作记忆、焦虑样行为,并分析了前额叶皮质炎症标志物(IL-6、IL-10和TNFα)、抗氧化酶(SOD、GSH和CAT)以及促氧化剂MDA水平。此外,我们对暴露于镉(2.5毫克/千克)的瑞士白化小鼠的前额叶皮质进行了组织学研究。我们观察到,姜黄素治疗通过减轻前额叶皮质神经炎症和氧化应激以及增加存活的前额叶皮质神经元细胞数量,改善了小鼠的空间工作记忆和焦虑样行为。我们的结果表明,环境重金属镉可通过前额叶皮质细胞炎症和氧化应激诱导小鼠行为障碍。我们发现姜黄素具有减轻镉诱导的这些行为和生化损伤的潜在治疗特性。