College of Food Science and Technology, School of Chemistry and Environment, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Shenzhen Insititute of Guangdong Ocean University, Guangdong Ocean University, Zhanjiang 524088, China.
Southern Marine Science and Engineering Guangdong Laboratory, Zhanjiang 524000, China.
Int J Mol Sci. 2023 Jan 4;24(2):905. doi: 10.3390/ijms24020905.
Alzheimer's disease (AD), a neurodegenerative disease, is the most common cause of dementia in humans worldwide. Although more in-depth research has been carried out on AD, the therapeutic effect of AD is not as expected, and natural active substances are increasingly sought after by scientists. In the present study, we evaluated two benzaldehydes from a coral-derived strain C23-3, their anti-neuroinflammatory activity in microglia (BV-2), and their neuroprotective activity and mechanisms in hippocampal neuronal cells (HT-22). These include the protein expression of iNOS, COX-2, MAPKs pathways, Tau protein-related pathways, caspases family-related signaling pathways. They also include the levels of TNF-α, IL-6, IL-18 and ROS, as well as the level of mitochondrial oxidative stress and neuronal cell apoptosis. The results showed that both benzaldehydes were effective in reducing the secretion of various inflammatory mediators, as well as pro-inflammatory factors. Among these, benzaldehyde inhibited mitochondrial oxidative stress and blocked neuronal cell apoptosis through Tau protein-related pathways and caspases family-related signaling pathways, thereby inhibiting β-amyloid (Aβ)-induced neurological damage. This study reveals that benzaldehyde has potential as a therapeutic agent for Alzheimer's disease, and offers a new approach to the high-value use of marine natural products.
阿尔茨海默病（AD）是一种神经退行性疾病，是全世界最常见的痴呆症病因。尽管对 AD 进行了更深入的研究，但 AD 的治疗效果并不理想，天然活性物质越来越受到科学家的追捧。在本研究中，我们评估了两种来自珊瑚源菌株 C23-3 的苯甲醛，它们在小胶质细胞（BV-2）中的抗神经炎症活性，以及它们在海马神经元细胞（HT-22）中的神经保护活性和机制。这些包括 iNOS、COX-2、MAPKs 通路、Tau 蛋白相关通路、半胱天冬酶家族相关信号通路的蛋白表达。还包括 TNF-α、IL-6、IL-18 和 ROS 的水平，以及线粒体氧化应激和神经元细胞凋亡的水平。结果表明，两种苯甲醛都能有效减少各种炎症介质和促炎因子的分泌。其中，苯甲醛通过 Tau 蛋白相关通路和半胱天冬酶家族相关信号通路抑制线粒体氧化应激和阻断神经元细胞凋亡，从而抑制β-淀粉样蛋白（Aβ）诱导的神经损伤。本研究表明，苯甲醛具有作为治疗阿尔茨海默病的药物的潜力，为海洋天然产物的高值化利用提供了新途径。
Zotero 插件
