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一种新型硒多糖可减轻 Hep G2 细胞及. 中的锰(Mn)诱导的毒性。

A Novel Selenium Polysaccharide Alleviates the Manganese (Mn)-Induced Toxicity in Hep G2 Cells and .

机构信息

College of Life Science, Sichuan Agricultural University, Ya'an 625014, China.

出版信息

Int J Mol Sci. 2022 Apr 7;23(8):4097. doi: 10.3390/ijms23084097.

Abstract

Manganese (Mn) is now known to have a variety of toxicities, particularly when exposed to it in the workplace. However, there are still ineffective methods for reducing Mn's hazardous effects. In this study, a new selenium polysaccharide (Se-PCS) was developed from the shell of to reduce Mn toxicity in vitro and in vivo. The results revealed that Se-PCS may boost cell survival in Hep G2 cells exposed to Mn and activate antioxidant enzyme activity, lowering ROS and cell apoptosis. Furthermore, after being treated with Se-PCS, survived longer under Mn stress. , a tolerant critical gene, was turned on. Moreover, the antioxidant system was enhanced as the increase in strong antioxidant enzyme activity and high expression of the , , and genes. A variety of mutations were also used to confirm that Se-PCS downregulated the insulin signaling pathway. These findings showed that Se-PCS protected Hep G2 cells and via the insulin/IGF-1 signaling pathway and that it could be developed into a promising medication to treat Mn toxicity.

摘要

锰 (Mn) 现在被认为具有多种毒性,特别是在工作场所接触时。然而,目前仍然缺乏有效方法来降低 Mn 的危害性。在这项研究中,一种从贻贝壳中提取的新型硒多糖 (Se-PCS) 被开发出来,以减少体内外 Mn 的毒性。结果表明,Se-PCS 可能会促进暴露于 Mn 中的 Hep G2 细胞的存活并激活抗氧化酶活性,降低 ROS 和细胞凋亡。此外,用 Se-PCS 处理后, 在 Mn 胁迫下存活时间更长。耐关键基因被打开。此外,抗氧化系统增强,因为强抗氧化酶活性增加和 、 、 和 基因的高表达。还使用了多种突变来证实 Se-PCS 下调了胰岛素信号通路。这些发现表明,Se-PCS 通过胰岛素/IGF-1 信号通路保护 Hep G2 细胞和 ,并且它可以被开发成一种有前途的药物来治疗 Mn 毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f723/9029073/197ea9cf2804/ijms-23-04097-g001.jpg

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