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多糖通过p38丝裂原活化蛋白激酶信号通路对Aβ诱导的PC12细胞损伤的神经保护作用

Neuroprotective Effect of Polysaccharide on Aβ-Induced Damage in PC12 Cells via the p38MAPK Signaling Pathways.

作者信息

Yang Liu, Song Shiyi, Li Xinlu, Wang Jinquan, Bao Yanan, Wang Xinxin, Lian Liwei, Liu Xiubo, Ma Wei

机构信息

College of Pharmacy, Heilongjiang University of Chinese Medicine, Harbin 150040, China.

College of Jiamusi, Heilongjiang University of Chinese Medicine, Jiamusi 154007, China.

出版信息

Pharmaceuticals (Basel). 2024 Sep 18;17(9):1231. doi: 10.3390/ph17091231.

Abstract

OBJECTIVES

Plant polysaccharides have attracted increasing attention due to their high efficiency and low toxicity. polysaccharide (CPP) is an essential substance extracted from , 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-induced damage in PC12 cells and its underlying molecular mechanisms.

METHODS

The neuroprotective effect of CPP was evaluated using Aβ-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 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 induction.

RESULTS

The CPP markedly inhibited Aβ-induced reduction in the viability and apoptosis of PC12 cells. CPP also reduced the Aβinduced increase in the expression of the apoptosis factors and the levels of free radicals (ROS and MDA) and reversed the Aβ-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-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.

摘要

目的

植物多糖因其高效低毒而受到越来越多的关注。壳聚糖磷酸酯(CPP)是从[具体来源未给出]中提取的一种重要物质,以其优异的抗氧化和神经保护作用而闻名。然而,CPP如何改善神经保护作用及其潜在的分子机制仍不清楚。本研究旨在探讨CPP对Aβ诱导的PC12细胞损伤的神经保护作用及其潜在的分子机制。

方法

以Aβ诱导的嗜铬细胞瘤(PC12)细胞损伤作为体外细胞模型,评估CPP的神经保护作用。在Aβ培养中,细胞单独用CPP处理或与SB203580(p38丝裂原活化蛋白激酶抑制剂)联合处理。使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)法评估细胞活力。此外,使用流式细胞术检测活性氧(ROS)。采用比色法测定细胞内超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、过氧化氢酶(CAT)和丙二醛(MDA)的产生水平。使用荧光显微镜进行膜联蛋白V-异硫氰酸荧光素(Annexin V-FITC)和碘化丙啶(PI)染色以及[此处“33258”可能有误,未明确其准确含义]检测。此外,研究添加SB203580的效果,以确定CPP处理和Aβ诱导所引起的细胞凋亡变化。

结果

CPP显著抑制Aβ诱导的PC12细胞活力降低和凋亡。CPP还降低了Aβ诱导的凋亡因子表达增加以及自由基(ROS和MDA)水平,并逆转了Aβ诱导的抗氧化活性抑制。此外,通过添加拮抗剂抑制p38丝裂原活化蛋白激酶可逆转观察到的CPP的抗凋亡作用。

结论

CPP可以有效地针对Aβ诱导的PC12细胞氧化和凋亡反应损伤提供神经保护,其潜在机制涉及p38丝裂原活化蛋白激酶途径。因此,CPP在天然药物、制药和食品工业中可能作为一种神经保护剂具有潜在用途。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b33b/11435206/f98956d909e8/pharmaceuticals-17-01231-g001a.jpg

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