2. Academic Validation
  3. Phenolic C-Glycosides and Aglycones from Marine-Derived Aspergillus sp. and Their Anti-Inflammatory Activities

Phenolic C-Glycosides and Aglycones from Marine-Derived Aspergillus sp. and Their Anti-Inflammatory Activities

  • J Nat Prod. 2019 May 24;82(5):1098-1106. doi: 10.1021/acs.jnatprod.8b00744.
Huiling Wen 1 2,  Chunmei Chen 1,  Weiguang Sun 1,  Yi Zang 1,  Qin Li 1,  Wenxuan Wang 3,  Fanrong Zeng 1,  Junjun Liu 1,  Yuan Zhou 1,  Qun Zhou 1,  Jianping Wang 1,  Zengwei Luo 1,  Hucheng Zhu 1,  Yonghui Zhang 1
Affiliations

Affiliations

  • 1 Hubei Key Laboratory of Natural Medicinal Chemistry and Resource Evaluation and Department of Pharmacology, School of Pharmacy, Tongji Medical College , Huazhong University of Science and Technology , Wuhan 430030 , People's Republic of China.
  • 2 School of Pharmaceutical Sciences , Gannan Medical University , Ganzhou 341000 , People's Republic of China.
  • 3 School of Pharmaceutical Sciences , South-Central University for Nationalities , Wuhan , Hubei 430074 , People's Republic of China.
PMID: 31012585 DOI: 10.1021/acs.jnatprod.8b00744
Abstract

A chemical investigation of the secondary metabolites of a marine-derived Aspergillus sp. led to the isolation and characterization of 13 phenolic compounds, including 10 new compounds (1-10). Seven new compounds (1-7) are unusual phenolic C-glycosides, while the Other new compounds (8-10) are structurally related aglycones. The chemical structures of these new compounds were elucidated by 1D and 2D NMR and HRESIMS spectroscopic analyses. The absolute configurations of these new C-glycosides were determined by comparison of experimental electronic circular dichroism spectra with those of calculated ones. In addition, the anti-inflammatory activities of these compounds were evaluated, and compound 9 significantly inhibited nitric oxide production with an IC50 value of 6.0 ± 0.5 μM in lipopolysaccharide-induced RAW264.7 cells. Moreover, compound 9 also showed anti-inflammatory activity by inhibiting the NF-κB-activated pathway.

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