Lithocarpins E-G,featuring a rare naturally-occurring highly oxygenated tenellone-macrolide skeleton,were isolated from the culture extract of a marine-derived fungus Phomopsis lithocarpus FS508.Their structures were ...Lithocarpins E-G,featuring a rare naturally-occurring highly oxygenated tenellone-macrolide skeleton,were isolated from the culture extract of a marine-derived fungus Phomopsis lithocarpus FS508.Their structures were fully elucidated by NMR and MS spectroscopic analyses and electronic circular dichroism calculations.Compounds 1-3 were evaluated for their in vitro cytotoxicities against HepG2,MCF-7,SF-268,as well as A549 cell lines,among which,compound 1 exhibited inhibitory activity against HepG2 cells with an IC_(50) value of 6.3 μmol/L.The further mechanistic investigation demonstrated that lithocarpin E could cause the apoptosis of HepG2 cells through activation of p-ERK,Bax,and caspase-3 gene expressions.展开更多
基金Guangdong Provincial Special Fund for Marine Economic Development Project([2020]042)the National Natural Science Foundation of China(41906106)+3 种基金the Guangdong Special Support Program(2019TQ05Y375)Team Project of the Natural Science Foundation of Guangdong Province(2016A030312014)the GDAS_Project of Science and Technology Development(2019GDASYL-0103007)We sincerely thank Mr.Can Li of central laboratory of Southern Medical University for NMR measurements.
文摘Lithocarpins E-G,featuring a rare naturally-occurring highly oxygenated tenellone-macrolide skeleton,were isolated from the culture extract of a marine-derived fungus Phomopsis lithocarpus FS508.Their structures were fully elucidated by NMR and MS spectroscopic analyses and electronic circular dichroism calculations.Compounds 1-3 were evaluated for their in vitro cytotoxicities against HepG2,MCF-7,SF-268,as well as A549 cell lines,among which,compound 1 exhibited inhibitory activity against HepG2 cells with an IC_(50) value of 6.3 μmol/L.The further mechanistic investigation demonstrated that lithocarpin E could cause the apoptosis of HepG2 cells through activation of p-ERK,Bax,and caspase-3 gene expressions.
