Artemiprincepsolides A—F, Novel Germacrane‐guaiane and Eudesmane‐guaiane Sesquiterpenoid Dimers from Artemisia princeps and Their Antihepatoma Activity

• Published in: Chinese journal of chemistry Vol. 41; no. 20; pp. 2648 - 2656
• Main Authors: Su, Li‐Hua, Ma, Wen‐Jing, Ma, Yun‐Bao, Li, Tian‐Ze, Geng, Chang‐An, Dong, Wei, He, Xiao‐Feng, Zhang, Xue‐Mei, Chen, Ji‐Jun
• Format: Journal Article
• Language: English
• Published: WEINHEIM Wiley 15.10.2023; Wiley Subscription Services, Inc
• Subjects: Adducts; Apoptosis; Artemisia princeps; Biocompatibility; Biological activity; Cell lines; Cell migration; Chemistry; Chemistry, Multidisciplinary; Cycloaddition; Cytotoxicity; Dimers; Flow cytometry; Hepatoma; Physical Sciences; Proteins; Science & Technology; Toxicity; Antihepatoma activity; Artemiprincepsolides; JACEOSIDIN; Artemisia princeps; Stereochemistry; Structure elucidation; Hetero-coupled sesquiterpenoid dimers; Biological activity; Apoptosis
• ISSN: 1001-604X; 1614-7065
• DOI: 10.1002/cjoc.202300242

Artemiprincepsolides A—F ( 1 — 6 ) were isolated from Artemisia princeps guided by bioactivity and elucidated by comprehensive spectral data and ECD calculation. Compounds 1 — 3 represented the first connecting model of germacrane‐guaiane hetero‐dimeric adducts, and compounds 4 — 6 were eudesmane‐guaiane hetero‐coupled sesquiterpenoid dimers, meanwhile, all these were presumably formed by Diels‐Alder cycloaddition. Compounds 1 — 6 were evaluated for their hepatomatic cytotoxicity on three hepatoma cell lines, and demonstrated cytotoxicity with IC 50 values in the range of 5.0—67.3 μmol/L. Interestingly, compound 1 manifested significant cytotoxicity against HepG2, Huh7, and SK‐Hep‐1 cells with IC 50 values of 9.9, 9.2, and 5.0 μmol/L, which were almost equivalent to the positive control, sorafenib. Flow cytometry data and Western blot assays revealed the most active compound 1 dose‐dependently inhibited cell migration and invasion, and significantly induced HepG2 cells arrest in G2/M phase by downregulating proteins pcdc2 and upregulating the level of protein CyclinB1; and induced apoptosis by downregulating of Bcl‐2 expression and upregulating Bax level.