陈年六堡茶对Aβ25-35诱导的PC12细胞损伤的神经保护研究

doi:10.13305/j.cnki.jts.20241203.001

茶叶科学 ›› 2024, Vol. 44 ›› Issue (6): 1005-1013.doi: 10.13305/j.cnki.jts.20241203.001

陈年六堡茶对Aβ_25-35诱导的PC12细胞损伤的神经保护研究

聂晴¹, 庞月兰^2,*, 吴焕¹, 丁树洽¹, 钟可渝¹, 刘仲华¹, 蔡淑娴^1,*

1.国家植物功能成分利用工程技术研究中心,湖南农业大学茶学教育部重点实验室,湖南长沙 410128;
2.广西壮族自治区茶叶科学研究所,桂林茶树资源广西野外科学观测研究站,广西桂林 541004

收稿日期:2024-08-15 修回日期:2024-09-16 出版日期:2024-12-15 发布日期:2025-01-08
通讯作者: *pyl_2005@163.com;caishuxian@hunau.edu.cn
作者简介:聂晴,女,硕士研究生,从事茶叶深加工与资源高值化利用方面研究。
基金资助:
广西创新驱动发展专项资金项目（AA20302018）、广西茶叶试验站（TS202106）、国家重点研发计划（2018YFC1604405）、国家自然科学基金项目（31471590、31100501）

Neuroprotective Mechanisms of Aged Liupao Tea against Aβ_25-35-induced PC12 Cell Damage

NIE Qing¹, PANG Yuelan^2,*, WU Huan¹, DING Shuqia¹, ZHONG Keyu¹, LIU Zhonghua¹, CAI Shuxian^1,*

1. National Research Center of Engineering and Technology for Utilization of Botanical Functional Ingredients, Key Lab of Education Ministry of Hunan Agricultural University for Tea Science, Changsha 410128, China;
2. Guangxi Research Institute of Tea Science, Guangxi Field Scientific Observation and Research Station for Tea Resources, Guilin 541004, China

Received:2024-08-15 Revised:2024-09-16 Online:2024-12-15 Published:2025-01-08

摘要/Abstract

摘要： 通过建立β-淀粉样蛋白_25-35（Aβ_25-35）诱导的PC12细胞损伤模型,以绿茶（GT）为对照,探讨了陈年六堡茶（ALPT）对神经细胞的保护作用及机制。研究结果表明,Aβ_25-35会导致PC12细胞的活性下降,诱发线粒体功能障碍、诱导有毒集聚物及其通路的形成。ALPT干预显著提高了PC12细胞的存活率及其线粒体膜电位,并显著抑制了有毒集聚物积累及其通路的形成。转录组分析显示,ALPT处理组的基因表达整体趋势与Aβ_25-35组相反,上调基因与线粒体自噬、糖酵解、甘油磷脂代谢相关;下调基因主要参与细胞周期调控、核糖体功能、泛素介导的蛋白质水解及细胞衰老过程。总体而言,GT与ALPT均具有显著抑制Aβ_25-35诱导的PC12细胞损伤作用,在转录组水平上影响作用差别较大,这可能与ALPT活性成分具有更好的生物利用度有关。研究结果可为陈年六堡茶在神经退行性疾病预防和治疗中的应用提供试验依据。

关键词: 陈年六堡茶, β-淀粉样蛋白_25-35, PC12细胞, 神经保护, 线粒体功能

Abstract: In this study, an Aβ_25-35-induced PC12 cell damage model was established to investigate the neuroprotective effects and underlying mechanisms of aged Liupao tea (ALPT), with green tea (GT) as a reference. The results show that Aβ_25-35 significantly reduced PC12 cell viability, induced mitochondrial dysfunction, and promoted the formation of toxic aggregates and related pathways. ALPT markedly improved cell survival, increased mitochondrial membrane potential, and significantly inhibited the accumulation of toxic aggregates and the formation of related pathways. Furthermore, transcriptome analysis reveals that the overall gene expression pattern in the ALPT treatment group was the opposite to that in the Aβ_25-35 group, with upregulated genes involved in mitophagy, glycolysis and glycerophospholipid metabolism, and downregulated genes associated with cell cycle regulation, ribosomal function, ubiquitin-mediated proteolysis and cellular senescence. Overall, both GT and ALPT exhibited significant protective effects against Aβ_25-35-induced PC12 cell damage, though transcriptomic differences suggest that ALPT may have superior bioavailability due to its active components. This study provided experimental evidence for the potential application of ALPT in the prevention and treatment of neurodegenerative diseases.

Key words: aged Liupao tea, Aβ_25-35, PC12 cells, neuroprotective, mitochondrial function

中图分类号:

S571.1
R741

聂晴, 庞月兰, 吴焕, 丁树洽, 钟可渝, 刘仲华, 蔡淑娴. 陈年六堡茶对Aβ_25-35诱导的PC12细胞损伤的神经保护研究[J]. 茶叶科学, 2024, 44(6): 1005-1013. doi: 10.13305/j.cnki.jts.20241203.001.

NIE Qing, PANG Yuelan, WU Huan, DING Shuqia, ZHONG Keyu, LIU Zhonghua, CAI Shuxian. Neuroprotective Mechanisms of Aged Liupao Tea against Aβ_25-35-induced PC12 Cell Damage[J]. Journal of Tea Science, 2024, 44(6): 1005-1013. doi: 10.13305/j.cnki.jts.20241203.001.

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陈年六堡茶对Aβ_25-35诱导的PC12细胞损伤的神经保护研究

Neuroprotective Mechanisms of Aged Liupao Tea against Aβ_25-35-induced PC12 Cell Damage

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陈年六堡茶对Aβ25-35诱导的PC12细胞损伤的神经保护研究

Neuroprotective Mechanisms of Aged Liupao Tea against Aβ25-35-induced PC12 Cell Damage

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陈年六堡茶对Aβ_25-35诱导的PC12细胞损伤的神经保护研究

Neuroprotective Mechanisms of Aged Liupao Tea against Aβ_25-35-induced PC12 Cell Damage