VOLUME 15 NUMBER 2 (July to December 2022)

Jessa Mae M. Laude¹^, Myra Ruth D. Picart¹^, Albebson L. Lim¹^, Jortan O. Tun¹^, Cydee Marie V. Ramones¹^, Klidel Fae B. Rellin², Meljune O. Chicote¹, Eliza L. Belen¹, Ranjala Ratnayakeo³, James H. Matthews³, Hendrik Luesch³, Lilibeth A. Salvador-Reyes¹ and Gisela P. Concepcion*¹

¹The Marine Science Institute, University of the Philippines, Diliman,
      Quezon City 1101, Philippines
²Institute of Chemistry, University of the Philippines,
     Diliman, Quezon City 1101, Philippines
³Department of Medicinal Chemistry, University of Florida,
     Gainesville, Florida, U.S.A.

^contributed equally to the study

KEYWORDS: Moringa oleifera, glucosinolates from seeds, syrup formulation of leaf extract with flavonoids, anticancer and cancer chemopreventive properties

There is significant interest to use Moringa oleifera or “malunggay” as a source of anticancer and cancer chemopreventive agents to develop pharmaceutical drugs and herbal preparations. In this study, we isolated niazirin, niazinin, niazimicin, niaziminin and other glucosinolates, i.e., nitrile and O-thiocarbamate glycosides, from the ethanolic extract of M. oleifera seeds. These compounds were tested for antiproliferative activity in the MTT assay in human cancer cell lines, apoptotic activity in the annexin V/propidium iodide (PI) assay, antimigration activity in the matrigel wound healing assay, antiangiogenesis activity in the in ovo chorioallantoic membrane (CAM) assay, and activation of antioxidant response elements (ARE) in the ARE-luciferase reporter assay. The following activities were observed in the following compounds from seeds: antimigration and antiangionesis in niazirin; antimigration in niazinin; apoptosis, antimigration and antiangionesis in niazimicin; and antiproliferation and apoptosis in niaziminin. Several seed and leaf fractions activated ARE. We prepared a syrup formulation from an ethanolic leaf extract found to contain flavonoids, lipids and derivatives and a tetrapyrrole, which activated ARE and selectively inhibited SKOV-3 ovarian cancer cell line proliferation and showed no inhibition of the MDCK normal cell line.