郭孝萱,曹越维,夏 冰,廖光琴,董 颖,邱 静.红景天苷改善镉致神经损伤的作用机制研究[J].食品安全质量检测学报,2024,15(18):139-147
红景天苷改善镉致神经损伤的作用机制研究
Protecting mechanisms of salidroside in ameliorating cadmium-induced nerve injury
投稿时间:2024-07-16  修订日期:2024-09-06
DOI:
中文关键词:  红景天苷    神经毒性  凋亡  氧化应激  脂质组学
英文关键词:Salidroside, Cadmium, Neurotoxicity, Apoptosis, Oxidative  stress, Lipidomic
基金项目:中央级公益性科研院所基本科研业务费专项 (1610072023008);中国农业科学院农业科技创新计划(CAAS-ASTIP-IQSTAP-06)。
作者单位
郭孝萱 中国农业科学院农业质量标准与检测技术研究所 
曹越维 中国农业科学院农业质量标准与检测技术研究所 
夏 冰 中国农业科学院农业质量标准与检测技术研究所 
廖光琴 中国农业科学院农业质量标准与检测技术研究所 
董 颖 黄河科技学院 
邱 静 中国农业科学院农业质量标准与检测技术研究所 
AuthorInstitution
Guo Xiao Xuan Institute of Quality Standard and Testing Technology for Agro-products 
Yuewei Cao Institute of Quality Standard and Testing Technology for Agro-products 
Bing Xia Institute of Quality Standard and Testing Technology for Agro-products 
Guangqin Liao Institute of Quality Standard and Testing Technology for Agro-products 
Ying Dong Huanghe University of Science and Technology 
Jing Qiu Institute of Quality Standard and Testing Technology for Agro-products 
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中文摘要:
      为探明红景天苷对镉致神经损伤的保护作用,利用大鼠PC12神经细胞,分析红景天苷对镉致神经细胞存活率、细胞凋亡及氧化应激的影响。通过利用流式细胞仪和相关试剂盒,证明红景天苷可以改善高浓度镉暴露所致细胞存活率下降、抑制细胞Caspase-3酶活升高。同时红景天苷可以有效抑制镉诱导细胞活性氧Reactive Oxygen Species, ROS)产生,提高线粒体膜电位,减少早期凋亡细胞的比例、增加正常细胞的比例。通过脂质组学,揭示红景天苷作用下差异甘油磷脂包括PC(16:0/14:0)、PC(16:0/18:2)、PC(18:1/16:0)、PE(16:0/18:1)、PE(16:0/18:2)、PE(18:0/18:2)、PI(16:0/18:1)、PI(18:1/18:1)、PI(18:0/20:4)。该研究初步阐明了红景天苷可能通过抗氧化、抗凋亡等机制保护镉致神经细胞损伤,且其作用可能与部分甘油磷脂有关。该项研究可以为开发红景天苷的保健新用途提供科学依据。
英文摘要:
      In order to investigate the protective effect of salidroside on cadmium-induced nerve injury, the effects of salidroside on cadmium-induced decreased survival rate, increased apoptosis and oxidative stress in rat PC12 nerve cells were analyzed. By using flow cytometry and related kits, salidroside was shown to improve cell survival and inhibit cell Caspase-3 activity induced by high cadmium exposure. Meanwhile, salidroside can effectively inhibit cadmium-induced reactive oxygen species (ROS)production, increase mitochondrial membrane potential, reduce the proportion of early apoptotic cells and increase the proportion of normal cells. Finally, through lipidomics, it was revealed that the differential phospholipids in salidroside group include PC(16:0/14:0), PC(16:0/18:2), PC(18:1/16:0), PE(16:0/18:1), PE(16:0/18:2), PE(18:0/18:2), PI(16:0/18:1), PI(18:1/18:1), PI(18:0/20:4). This study clarified that salidroside may protect cadmium-induced nerve cell damage through anti-oxidation and anti-apoptosis mechanisms, and its effects may be related to differential glycerophospholipids. This study can provide scientific basis for developing new health care uses of salidroside.
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