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通过通过依赖于CUL3的AMPK/ULK1通路增强线粒消化,PF保护视网膜色素上皮细胞免受氧化损伤

Xi Chen¹, Wei Shi¹, Yujie Zhu¹

¹Affiliated Hospital of Nanjing University of Chinese Medicine, No. 155 Hanzhong Road, Qinhuai District, Nanjing, 210029, Jiangsu Province, P. R. China.

Archives of pharmacal research

|February 1, 2026

概括

佩奥尼弗洛林 (PF) 通过通过CUL3/LKB1/AMPK/ULK1通路增强线粒消化,保护视网膜色素上皮细胞 (RPE). 这项研究揭示了PF PF.

科学领域:

线粒体生物学线粒体生物学
细胞应激反应的细胞应激反应
神经保护是一种神经保护.

背景情况:

线粒功能障碍有助于视网膜退行性疾病,如与年龄相关的黄斑退行 (AMD).
视网膜色素上皮细胞 (RPE) 对于视网膜健康至关重要,易受损伤.
向线粒菌为RPE保护提供了一种治疗策略.

研究的目的:

为了研究 paeoniflorin (PF) 对 RPE 细胞中线粒的作用.
阐明CUL3/LKB1/AMPK/ULK1信号通路在PF介导的RPE保护中的作用.
在RPE损伤的体外和体内模型中评估PF的疗效.

主要方法:

使用ARPE-19细胞和酸 (NaIO3) 诱导的小鼠模型.
西方涂抹评估了CUL3的蛋白质水平,细胞亡因子,线粒的标志物,以及LKB1/AMPK/ULK1通路.
标记MitoTracker可视化了线粒;循环赫西米德和共免疫沉试验分析了蛋白质相互作用.

主要成果:

PF治疗增强了氧化应激诱导的RPE细胞中的线粒细胞衰变,缓解了线粒体功能障碍.
PF促进了LKB1/AMPK/ULK1的酸化和髓,这种效应取决于CUL3的下调.
在体内,PF防止了RPE细胞损失,并激活了AMD类模型中的CUL3/LKB1/AMPK/ULK1通路.

结论:

佩奥尼佛林通过降低CUL3表达的调节来保护RPE细胞免受损伤.
PF激活了LKB1/AMPK/ULK1介导的线粒,为AMD提供了潜在的治疗方法.
CUL3/LKB1/AMPK/ULK1轴是PF对RPE细胞的保护作用的关键调解器.

关键词:

在ARPE-19细胞中.与年龄相关的黄斑变性 (AMD)在 CUL3 中,我们可以使用 CUL3 .在LKB1/AMPK/ULK1中.佩奥尼佛洛林 (PF) 是一种视网膜色素上皮质 (RPE) 是一种

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