Bioassay-Guided Isolation of 2-[p-(2-Carboxyhydrazino)phenoxy]-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol from Oroxylum indicum and the Investigation of Its Molecular Mechanism Action of Apoptosis Induction

Abstract

The leaf crude extract of Oroxylum indicum (L.) Kurz induces genomic DNA fragmentation, comet formation, and the inhibition of cell proliferation in the prostate cancer cell line PC3, as assessed by agarose gel electrophoresis, comet assay and MTT assay, respectively. The bioactive compound was purified through bioassay-guided fractionation using preparative HPLC and MTT assay. The light brown and water-soluble compound was characterized using 1H and 13C nuclear magnetic resonance (NMR), Fourier transform infrared (FT-IR), and electrospray ionization (ESI) mass spectrometry. The compound was identified as a glycosylated hydroquinone derivative, 2-[p-(2-Carboxyhydrazino)phenoxy]-6-(hydroxymethyl) tetrahy-dro-2H-pyran-3,4,5-triol (molecular formula, C13H18N2O8; molecular mass = 330). The identified phytocompound has not been reported earlier elsewhere. Therefore, the common name of the novel anticancer phytocompound isolated from Oroxylum indicum in this current study is oroxyquinone. The half-maximal inhibitory concentration (IC50) of oroxyquinone on PC3 cells was 58.9 µM (95% CI = 54.5 to 63.7 µM). Treatment of PC3 cells with oroxyquinone induced genomic DNA fragmentation and chromatin condensation, increased in the annexin-V positive cells, arrested the cell cycle at S phases, and inhibited the cell migration; as assessed by comet assay, DAPI staining, flow cytometry and a wound healing assay, respectively. On the investigation of the molecular mechanism of the induction of apoptosis, the results indicated that oroxyquinone induced caspase-3 and PARP independent apoptosis but through the p38 pathway and the localization of AIF into the nucleus. The present study identifies a novel anticancer molecule and provides scientific evidence supporting the therapeutic potency of Oroxylum indicum for ethnomedicinal uses.

Screen time of children with speech delay: a cross‐sectional study in a tertiary center in Kuantan, Malaysia

“…The SGS‐II was validated in 2006 in a pilot study by the Family Health Development Division, Ministry of Health Malaysia. The sensitivity of the test was 0.44–0.82, while its specificity was 0.94–1.0, comparable with other developmental assessment tools such as the Denver Developmental Assessment (DDA) 17–19 . An excellent level of correlation between MSGS and DDA was also noted (0.87, P < 0.001), while the inter‐item and intra‐class reliability showed a Cronbach's Alpha of 0.98 and 0.86, respectively 18…”

“…The sensitivity of the test was 0.44-0.82, while its specificity was 0.94-1.0, comparable with other developmental assessment tools such as the Denver Developmental Assessment (DDA). [17][18][19] An excellent level of correlation between MSGS and DDA was also noted (0.87, P < 0.001), while the inter-item and intra-class reliability showed a Cronbach's Alpha of 0.98 and 0.86, respectively. 18 After the assessment, parents who reported children with excessive screen time would be given psychoeducation on appropriate screen use and supervision.…”