通过建立β-淀粉样蛋白25-35（Aβ25-35）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,Aβ25-35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Aβ25-35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Aβ25-35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。
In this study, an Aβ25-35-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 Aβ25-35 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 Aβ25-35 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 Aβ25-35-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.
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