Background. Aβ deposition abnormally in the mitochondria can damage the mitochondrial respiratory chain and activate the mitochondrial-mediated apoptosis pathway, resulting in AD-like symptoms. Objective. To observe the protective effects of Dendrobium nobile Lindl. alkaloids (DNLA) on Aβ_25-35-induced oxidative stress and apoptosis in PC12 cells explore its possible protective mechanisms. Methods. PC12 cells were treated with DNLA with different concentrations (0.035 mg/L, 0.3 mg/L, and 3.5 mg/L) for 6 h, followed by administration with Aβ_25-35 (10 μM) for 24 h. MTT assay and flow cytometer observe the effect of DNLA on Aβ_25-35-induced cytotoxicity and apoptosis of PC12 cell. Based on the mitochondrial apoptosis pathway to study the antiapoptotic effect of DNLA on this model and its relationship with oxidative stress, flow cytometer detected the level of reactive oxygen species (ROS), and ELISA kits were used to detect superoxide dismutase activity (SOD) and glutathione (GSH) content in cells. The JC-1 fluorescent staining observed the effect of DNLA on the mitochondrial membrane potential (MMP) with inverted immunofluorescence microscopy. Western blot was used to detect the levels of mitochondrial apoptosis pathway-related protein and its major downstream proteins Bax, Bcl-2, cleaved-caspase-9, and cleaved-caspase-3. Results. DNLA can significantly improve the viability and apoptosis rate of PC12 cell damage induced by Aβ_25-35. It also can restore the reduced intracellular ROS content and MMP, while SOD activity and GSH content increase significantly. The expression of apoptosis-related protein Bax, cleaved-caspase-9, and cleaved-caspase-3 decreased when the Bcl-2 protein expression was significantly increased. Conclusion. These findings suggest that it can significantly inhibit the apoptosis of PC12 cell damage induced by Aβ_25-35. The mechanism may reduce the level of cellular oxidative stress and thus inhibit the mitochondrial-mediated apoptosis pathway.

中文翻译：

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石斛的保护作用及机制。生物碱对 Aβ25-35 诱导的 PC12 细胞损伤的影响

背景。线粒体中的β沉积异常可破坏线粒体呼吸链并激活线粒体介导的细胞凋亡途径，导致AD样症状。客观的。观察金钗石斛的保护作用。_{生物碱（ DNLA}）对Aβ25-35诱导的PC12细胞氧化应激和凋亡的作用探索其可能的保护机制。方法。PC12 细胞用不同浓度（0.035 mg/L、0.3 mg/L 和 3.5 mg/L）的 DNLA 处理 6 h，然后用 A β _25-35 (10  μM) 24 小时。MTT法和流式细胞仪观察DNLA对_Aβ25-35诱导的PC12细胞细胞毒性和凋亡的影响。基于线粒体凋亡通路研究DNLA对该模型的抗凋亡作用及其与氧化应激的关系，流式细胞仪检测活性氧（ROS）水平，ELISA试剂盒检测超氧化物歧化酶活性（SOD）和细胞中的谷胱甘肽（GSH）含量。JC-1荧光染色用倒置免疫荧光显微镜观察DNLA对线粒体膜电位（MMP）的影响。Western blot检测线粒体凋亡通路相关蛋白及其主要下游蛋白Bax、Bcl-2、cleaved-caspase-9和cleaved-caspase-3的水平。结果。DNLA能显着提高Aβ25-35诱导的PC12细胞损伤的活力和凋亡_率。它还可以恢复降低的细胞内ROS含量和MMP，而SOD活性和GSH含量显着增加。当 Bcl-2 蛋白表达显着增加时，凋亡相关蛋白 Bax、cleaved-caspase-9 和 cleaved-caspase-3 的表达降低。结论。_{这些发现表明它可以显着抑制Aβ25-35}诱导的PC12细胞损伤的凋亡。该机制可能会降低细胞氧化应激水平，从而抑制线粒体介导的细胞凋亡途径。