Neuroprotective Effect of Codonopsis pilosula Polysaccharide on Aβ(25-35)-Induced Damage in PC12 Cells via the p38MAPK Signaling Pathways

党参多糖通过p38MAPK信号通路对Aβ(25-35)诱导的PC12细胞损伤的神经保护作用

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Abstract

OBJECTIVES: Plant polysaccharides have attracted increasing attention due to their high efficiency and low toxicity. Codonopsis pilosula polysaccharide (CPP) is an essential substance extracted from Codonopsis pilosula, known for its excellent antioxidant and neuroprotective effects. However, it is still unclear how CPP improves nerve protection and what its underlying molecular mechanisms are. This study aimed to investigate the neuroprotective effect of CPP on Aβ(25-35)-induced damage in PC12 cells and its underlying molecular mechanisms. METHODS: The neuroprotective effect of CPP was evaluated using Aβ(25-35)-induced damage in pheochFfromocytoma (PC12) cells as an in vitro cell model. The cells were treated with CPP alone or in combination with SB203580 (an inhibitor of p38MAPK) in Aβ(25-35) culture. The cell viability was assessed using a 3-(4,5-Dimethylthiazol-2-yl)-2,diphenyltetrazolium (MTT) assay. Furthermore, reactive oxygen species (ROS) were detected using flow cytometry. The production levels of intracellular superoxide dismutase (SOD), dismutase (SOD), glutathione (GSH), catalase (CAT), and malondialdehyFde (MDA) were determined using the colorimetric method. Annexin V-FITC and propidium iodide (PI) staining, as well as 33258 were performed using fluorescence microscopy. Moreover, the effect of adding SB203580 was studied to determine the changes in cell apoptosis induced by CPP treatment and Aβ(25-35) induction. RESULTS: The CPP markedly inhibited Aβ(25-35)-induced reduction in the viability and apoptosis of PC12 cells. CPP also reduced the Aβ(25-35-)induced increase in the expression of the apoptosis factors and the levels of free radicals (ROS and MDA) and reversed the Aβ(25-35)-induced suppression of antioxidant activity. Additionally, inhibition of p38MAPK via the addition of their antagonists reversed the observed anti-apoptosis effects of CPP. CONCLUSIONS: CPP can efficiently provide neuroprotection against Aβ(25-35)-induced damage in PC12 cells brought about via oxidation and apoptosis reactions, and the underlying mechanisms involve the p38MAPK pathways. Therefore, CPP could potentially be useful as a neuroprotective agent in natural medicine, pharmacy, and the food industry.

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