The methanol extract of Selaginella rolandi-principis was found to possess PTP1B inhibition. Thus, bioassay-guided separation of this active extract led to the isolation of four compounds (1–4) as active principles. | Vietnam Journal of Science and Technology 56 (4A) (2018) 69-73 TRITERPENOIDS FROM SELAGINELLA ROLANDI-PRINCIPIS AND THEIR PTP1B INHIBITORY ACTIVITY Nguyen Phi Hung1, 2, *, Nguyen Dinh Tuan1, 2, Pham Quoc Long1 1 Institute of Natural Products Chemistry, Vietnam Academy of Science and Technology (VAST), 18 Hoang Quoc Viet, Cau Giay, Ha Noi 2 Graduate University of Science and Technology, Vietnam Academy of Science and Technology (VAST), 18 Hoang Quoc Viet, Cau Giay, Ha Noi * Email: nguyenphihung1002@ Received: 30 July 2018; Accepted for publication: 10 October 2018 ABSTRACT As part of an ongoing search for new protein tyrosine phosphatese 1B (PTP1B) inhibitors from medicinal plants, the methanol extract of Selaginella rolandi-principis was found to possess PTP1B inhibition. Thus, bioassay-guided separation of this active extract led to the isolation of four compounds (1–4) as active principles. Their chemical structures were identified by extensive analysis of spectroscopic and physicochemical data. Among the isolates, compounds 1–3 exhibited potential inhibitory activities against PTP1B with IC50 values of ± , ± , and ± µM, respectively, against PTP1B. In this assay, ursolic acid as positive control displayed an IC50 value of µM. Keywords: Selaginella, Selaginella rolandi-principis, PTP1B inhibitor, tritepenoid, type-2 diabetes. 1. INTRODUCTION Protein tyrosine phosphatases 1B (PTP1B), a member of the PTP family, is thought to function as a negative regulator of insulin signal transduction. PTP1B directly interacts with activated insulin receptor or insulin receptor substrate-1 (IRS-1) to dephosphorylate phosphotyrosine residues, resulting in down regulation of insulin action [1]. PTP1B overexpression in rat primary adipose tissues and 3T3/L1 adipocytes has been shown to decrease insulin-sensitive Glut4 translocation [2] and insulin receptor and IRS-1 phosphorylation [3], respectively. Therefore, it has been suggested
