Abstract
Combretaceae plants are used traditionally by many cultures, especially in Sudanese patients for the treatment of diverse ailments such as anti-inflammatory, antimicrobial, antitumor, and antioxidant disorders. Of these plants, the genus Combretum are traditional medicinal plants. Thus, they are formed from the non-polar or polar extracts of many isolated phytochemicals. Of these necessities, the use of Combretum extracts for their medicinal properties can be found in the earliest of myths and traditions used to document the plants' ability to treat diseases. Combretum glutinosum Perr. Ex Dc. is a common shrub native to the African continent, especially Sudan. Currently, there are no published data regarding its cytotoxic activity. Additionally, there are few chemical and biological reports of C. glutinosum. Therefore, the current study aimed to isolate the chemical bioactive compounds (1-6) from the ethyl acetate (EtOAc) extract of C. glutinosum. A new flavonoid compound, namely, glutosinumoside (4), was afforded, and five known compounds were obtained: three oleanane-glycosides (1-3) and two phenolic acids (5,6). The structures of the six compounds were determined by spectroscopic analysis, including one- and two-dimensional (1D and 2D) NMR, mass spectrometry, and chromatographic analysis. Moreover, an in vitro cytotoxic evaluation of the successive extracts and the bioactive EtOAc fractions of C. glutinosum against MCF7 (breast), HT29 (colon), HepG2 (liver), and MRC5 (normal lung) cell lines was performed. The isolated compounds showed comparable cytotoxic activities with the crude EtOH extract and doxorubicin against the tested cell lines. Compounds (1) and (6) exhibited the highest cytotoxicity against MCF7 (1.37 +/- 0.21 and 1.48 +/- 0.34 mu g/mL, respectively) and HepG2 (3.30 +/- 0.02 and 2.10 +/- 0.22 mu g/mL, respectively) in the MTT assay. In addition, compounds (1) and (3) demonstrated a significant upregulation of cancer's two important hallmarks (caspase 3 and bax genes) by inducing apoptosis and perturbing the MCF7 cell cycle.