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海参精子多聚核苷酸对过氧化氢诱导 RAW264.7 细胞损伤模型的保护作用的蛋白质组学分析。

Proteomics Analysis of the Protective Effect of Polydeoxyribonucleotide Extracted from Sea Cucumber () Sperm in a Hydrogen Peroxide-Induced RAW264.7 Cell Injury Model.

机构信息

Department of Food Science and Technology, Shanghai Ocean University, Shanghai 200120, China.

Shandong Marine Resource and Environment Research Institute, Yantai 264006, China.

出版信息

Mar Drugs. 2024 Jul 21;22(7):325. doi: 10.3390/md22070325.

DOI:10.3390/md22070325
PMID:39057434
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11277713/
Abstract

Sea cucumber viscera contain various naturally occurring active substances, but they are often underutilized during sea cucumber processing. Polydeoxyribonucleotide (PDRN) is an adenosine A receptor agonist that activates the A receptor to produce various biological effects. Currently, most studies on the activity of PDRN have focused on its anti-inflammatory, anti-apoptotic, and tissue repair properties, yet relatively few studies have investigated its antioxidant activity. In this study, we reported for the first time that PDRN was extracted from the sperm of (AJS-PDRN), and we evaluated its antioxidant activity using 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2'-azino-bis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS), and hydroxyl radical scavenging assays. An in vitro injury model was established using HO-induced oxidative damage in RAW264.7 cells, and we investigated the protective effect of AJS-PDRN on these cells. Additionally, we explored the potential mechanism by which AJS-PDRN protects RAW264.7 cells from damage using iTRAQ proteomics analysis. The results showed that AJS-PDRN possessed excellent antioxidant activity and could significantly scavenge DPPH, ABTS, and hydroxyl radicals. In vitro antioxidant assays demonstrated that AJS-PDRN was cytoprotective and significantly enhanced the antioxidant capacity of RAW264.7 cells. The results of GO enrichment and KEGG pathway analysis indicate that the protective effects of AJS-PDRN pretreatment on RAW264.7 cells are primarily achieved through the regulation of immune and inflammatory responses, modulation of the extracellular matrix and signal transduction pathways, promotion of membrane repair, and enhancement of cellular antioxidant capacity. The results of a protein-protein interaction (PPI) network analysis indicate that AJS-PDRN reduces cellular oxidative damage by upregulating the expression of intracellular selenoprotein family members. In summary, our findings reveal that AJS-PDRN mitigates HO-induced oxidative damage through multiple pathways, underscoring its significant potential in the prevention and treatment of diseases caused by oxidative stress.

摘要

海参内脏含有各种天然存在的活性物质,但在海参加工过程中往往未被充分利用。聚脱氧核糖核苷酸 (PDRN) 是一种腺苷 A 受体激动剂,可激活 A 受体产生各种生物学效应。目前,大多数关于 PDRN 活性的研究都集中在其抗炎、抗凋亡和组织修复特性上,而相对较少的研究关注其抗氧化活性。在这项研究中,我们首次从 (AJS-PDRN) 的精子中提取出 PDRN,并使用 2,2-二苯基-1-苦基肼基 (DPPH)、2,2'-联氮-双-3-乙基苯并噻唑啉-6-磺酸 (ABTS) 和羟基自由基清除实验评估其抗氧化活性。我们使用 HO 诱导 RAW264.7 细胞氧化损伤建立了体外损伤模型,并研究了 AJS-PDRN 对这些细胞的保护作用。此外,我们通过 iTRAQ 蛋白质组学分析探索了 AJS-PDRN 保护 RAW264.7 细胞免受损伤的潜在机制。结果表明,AJS-PDRN 具有出色的抗氧化活性,可显著清除 DPPH、ABTS 和羟基自由基。体外抗氧化实验表明,AJS-PDRN 具有细胞保护作用,可显著增强 RAW264.7 细胞的抗氧化能力。GO 富集和 KEGG 通路分析的结果表明,AJS-PDRN 预处理对 RAW264.7 细胞的保护作用主要是通过调节免疫和炎症反应、调节细胞外基质和信号转导通路、促进膜修复和增强细胞抗氧化能力来实现的。蛋白质-蛋白质相互作用 (PPI) 网络分析的结果表明,AJS-PDRN 通过上调细胞内硒蛋白家族成员的表达来减轻细胞氧化损伤。综上所述,我们的研究结果表明,AJS-PDRN 通过多种途径减轻 HO 诱导的氧化损伤,突出了其在预防和治疗氧化应激引起的疾病方面的重要潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/3bc832d8e5f4/marinedrugs-22-00325-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/2f73b3d929a9/marinedrugs-22-00325-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/eddecca0b201/marinedrugs-22-00325-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/d1e447ccf8a8/marinedrugs-22-00325-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/5a9046e2d0b1/marinedrugs-22-00325-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/03b6a46844d4/marinedrugs-22-00325-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/b14ecfb4b4f7/marinedrugs-22-00325-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/3bc832d8e5f4/marinedrugs-22-00325-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/2f73b3d929a9/marinedrugs-22-00325-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/eddecca0b201/marinedrugs-22-00325-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/d1e447ccf8a8/marinedrugs-22-00325-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/5a9046e2d0b1/marinedrugs-22-00325-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/03b6a46844d4/marinedrugs-22-00325-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/b14ecfb4b4f7/marinedrugs-22-00325-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/11277713/3bc832d8e5f4/marinedrugs-22-00325-g007.jpg

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