网络毒理学,分子对接和分子动力学模拟,以探索非烯诱导心脏毒性的潜在机制
Nana Huang1, Yuanyuan Xiao1, Xiaoyue Zhang1
1School of Basic Medicine, Guizhou University of Traditional Chinese Medicine, Guiyang, China.
International journal of environmental health research
|October 5, 2025
概括
诺尼尔 (NP) 可能通过破坏PI3K-Akt和MAPK等关键细胞通路而导致心脏损伤. 这项研究使用了计算方法来确定NP的有毒目标和机制,有助于风险评估.
科学领域:
- 环境毒理学环境毒理学
- 计算生物学 计算生物学
- 心血管研究研究心血管研究
背景情况:
- 诺尼尔 (NP) 是一种环境污染物,可疑具有心脏毒性作用.
- 了解NP诱导心脏毒性的精确分子机制对于风险评估至关重要.
研究的目的:
- 用网络毒理学,分子对接和分子动力学模拟来阐明非烯诱导心脏毒性的机制.
- 为了确定关键的分子标和信号通路受影响的nonylphenol暴露在心脏.
主要方法:
- 利用Swisstarget预测,比较毒理学和Genecards数据库来识别197个潜在的目标基因.
- 使用STRING数据库和Cytoscape进行网络分析,以选8个核心目标 (例如AKT1,MAPK3,STAT3).
- 进行了基因本体学 (GO) 和KEGG通路丰富分析,分子对接和分子动力学模拟.
主要成果:
- 确定了8个核心目标,并发现NP主要影响PI3K-Akt,MAPK和JAK-STAT信号通路.
- 证明了NP与核心目标的稳定结合,特别是MAPK3,结合的自由能量为-1.215 kcal/mol.
- 证实了NP在调节细胞亡和炎症方面的作用,有助于心脏毒性.
结论:
- 诺尼尔可以通过干扰参与亡和炎症的关键信号通路来诱导心脏毒性.
- 这项研究为研究环境污染物的有毒机制提供了一个强大的计算框架.
- 这些发现为制定风险评估和预防NP相关心脏毒性策略奠定了理论基础.
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