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从思茅麻疯树的茎中提取具有潜在抗炎作用的木脂素和酚类化合物

Lignans and phenols with potential anti-inflammatory effect from the stems of Mallotus paxii Pamp.

机构信息

State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Collaborative Innovation Center for Guangxi Ethnic Medicine, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China; Guangxi Key Laboratory of Tradtitional Chinese Medicine Quality Standards, Guangxi Institute of Chinese Medicine & Pharmaceutical Science, Nanning 530022, China.

State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Collaborative Innovation Center for Guangxi Ethnic Medicine, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China.

出版信息

Fitoterapia. 2024 Dec;179:106253. doi: 10.1016/j.fitote.2024.106253. Epub 2024 Oct 11.

Abstract

Phytochemical investigation of the stems of Mallotus paxii Pamp. led to the isolation and identification of four new compounds, including three neolignans (1-3) and one phenol (13), along with eight known neolignans (4-12) and one known phenol (14). Their structures were determined by spectroscopic methods, including NMR, MS and ECD analyses. Bioassay demonstrated that malloapelin A (4) exhibited a most potent anti-inflammatory activity to NO release with IC value of 21.32 μM. Furthermore, malloapelin A (4) markedly decreased the secretion of TNF-α, iNOS, and NF-κB and inhibited the expression of COX-2 and NF-κB/p65 in LPS-induced RAW264.7 cells in a dose-dependent manner.

摘要

对思茅麻藤茎的化学成分研究,从中分离鉴定了 4 个新化合物,包括 3 个新木脂素(1-3)和 1 个酚类化合物(13),以及 8 个已知的新木脂素(4-12)和 1 个已知的酚类化合物(14)。它们的结构通过光谱方法,包括 NMR、MS 和 ECD 分析确定。生物测定表明,马罗阿品 A(4)对 NO 释放表现出最强的抗炎活性,IC 值为 21.32 μM。此外,马罗阿品 A(4)显著降低了 LPS 诱导的 RAW264.7 细胞中 TNF-α、iNOS 和 NF-κB 的分泌,并呈剂量依赖性抑制 COX-2 和 NF-κB/p65 的表达。

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