4.7 Article

New chromones from the roots of Saposhnikovia divaricata (Turcz.) Schischk with anti-inflammatory activity

Journal

BIOORGANIC CHEMISTRY
Volume 134, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bioorg.2023.106447

Keywords

Saposhnikovia divaricata; Chromone; Anti-inflammatory; RAW264; 7 cells

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Fifteen new chromones and fifteen known chromones were isolated from the roots of Saposhnikovia divaricata. Their structures were determined using NMR data and ECD calculations. The anti-inflammatory activity of these compounds was evaluated using an in vitro inflammatory cell model, and compounds 2, 8, 12-13, 18, 20-22, 24, and 27 showed significant inhibition of LPS-induced NO production. Mechanistic studies revealed that compounds 12 and 13 inhibited the phosphorylation of ERK and the activation of ERK and JNK signaling in RAW264.7 cells via MAPK signaling pathways. These findings suggest that compounds 12 and 13 may be potential candidates for the treatment of inflammatory diseases.
Fifteen new chromones, sadivamones A-E (1-5), cimifugin monoacetate (6), sadivamones F-N (7-15), together with fifteen known chromones (16-30), were isolated from the ethyl acetate portions of 70% ethanol extract of Saposhnikovia divaricata (Turcz.) Schischk roots. The structures of the isolates were determined using 1D/2D NMR data and electron circular dichroism (ECD) calculations. Meanwhile, LPS induced RAW264.7 inflammatory cell model was used to determine the potential anti-inflammatory activity of all the isolated compounds in vitro. The results showed that compounds 2, 8, 12-13, 18, 20-22, 24, and 27 significantly inhibited the production of lipopolysaccharide (LPS)-induced NO in macrophages. To determine the signaling pathways involved in the suppression of NO production by compounds 8, 12 and 13, we investigated ERK and c-Jun N-terminal protein kinase (JNK) expression by western blot analysis. Further mechanistic studies demonstrated that compounds 12 and 13 inhibited the phosphorylation of ERK and the activation of ERK and JNK signaling in RAW264.7 cells via MAPK signaling pathways. Taken together, compounds 12 and 13 may be valuable candidates for the treatment of inflammatory diseases.

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