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      Dalestones A and B, two anti-inflammatory cyclopentenones from Daldinia eschscholzii with an edited strong promoter for the global regulator LaeA-like gene

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          Abstract

          Replacement of the native promoter of the global regulator LaeA-like gene of Daldinia eschscholzii by a strong gpdA promoter led to the generation of two novel cyclopentenone metabolites, named dalestones A and B, whose structures were assigned by a combination of spectroscopic analysis, modified Mosher's reaction, and electronic circular dichroism (ECD). Dalestones A and B inhibit the gene expression of TNF- α and IL-6 in LPS-induced RAW264.7 macrophages.

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          Author and article information

          Journal
          CJNM
          Chinese Journal of Natural Medicines
          Elsevier
          1875-5364
          20 May 2019
          : 17
          : 5
          : 387-393
          Affiliations
          1 State Key Laboratory of Pharmaceutical Biotechnology, Institute of Functional Biomolecules, Nanjing University, Nanjing 210023, China
          2 State Key Laboratory Cultivation Base for TCM Quality and Efficacy, Nanjing University of Chinese Medicine, Nanjing 210023, China
          3 School of Pharmacy, Nanjing Medical University, Nanjing, 210029, China
          Author notes
          *Corresponding author: TAN Ren-Xiang, E-mail: rxtan@ 123456nju.edu.cn ; GE Hui-Ming, E-mail: hmge@ 123456nju.edu.cn

          ΔThese authors contributed equally to this work.

          These authors have no conflict of interest to declare.

          Article
          S1875-5364(19)30045-7
          10.1016/S1875-5364(19)30045-7
          Copyright © 2019 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
          Funding
          Funded by: National Natural Science Foundation of China
          Award ID: 21672101
          Award ID: 21702099
          Award ID: 81673333
          This work was supported by the National Natural Science Foundation of China (Nos. 21672101, 21702099 and 81673333).

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