RESUMEN
Penigrines A-E (1-5), five undescribed azepine-indole alkaloids, were isolated from the fungus Penicillium griseofulvum. Their structures with absolute configurations were determined by NMR, HRESIMS, ECD calculation, and X-ray diffraction experiments. Penigrine C (3) possesses an undescribed 6-oxa-8-azabicyclo[3.2.2]nonane-7,9-dione moiety that fused to an indole core, and penigrines D and E (4 and 5) are a pair of epimers. The plausible biosynthetic pathways of 1-5 are proposed. Penigrine A (1) shows the potential for heart failure treatment.
Asunto(s)
Alcaloides Indólicos , Penicillium , Alcaloides Indólicos/química , Penicillium/química , Espectroscopía de Resonancia Magnética , Hongos , Estructura MolecularRESUMEN
Six griseofulvin analogues named penigriseofulvins A - F (1-6), including three undescribed compounds and three undescribed natural products, were isolated from the fungus Penicillium griseofulvum. Their structures and absolute configurations were determined by NMR spectroscopic analyses, HRESIMS, and X-ray diffraction experiments. All compounds were evaluated for their anti-inflammatory activity, of which compounds 1 and 4 showed potential anti-inflammatory effects in RAW264.7 macrophages and ulcerative colitis mice.
Asunto(s)
Griseofulvina , Penicillium , Ratones , Animales , Griseofulvina/farmacología , Antiinflamatorios/farmacología , Penicillium/química , Espectroscopía de Resonancia Magnética , Estructura MolecularRESUMEN
Five new cyclopiazonic acid related indole alkaloids, pegriseofamines A-E (1-5), were isolated from the fungus Penicillium griseofulvum. Their structures and absolute configurations were determined by NMR, HRESIMS, quantum-chemical calculation, and X-ray diffraction experiments. Among them, pegriseofamine A (1) possesses an undescribed 6/5/6/7 tetracyclic ring system generated by the fusion of an azepine and an indole unit via a cyclohexane, and the postulated biosynthetic origin of 1 was discussed. Compound 4 could relieve liver injury and prevent hepatocyte apoptosis in ConA-induced autoimmune liver disease.