Moringa oleifera seed methanol extract with consolidated antimicrobial, antioxidant, anti‐inflammatory, and anticancer activities

Author:

El‐Fakharany Esmail M.123ORCID,Elsharkawy Wafaa B.4,El‐Maradny Yousra A.25,El‑Gendi Hamada6

Affiliation:

1. Protein Research Department, Genetic Engineering and Biotechnology Research Institute (GEBRI) City of Scientific Research and Technological Applications (SRTA‐City) New Borg El‐Arab City Alexandria Egypt

2. Pharmaceutical and Fermentation Industries Development Center City of Scientific Research and Technological Applications (SRTA‐City) New Borg El‐Arab City Alexandria Egypt

3. Pharos University in Alexandria Alexandria Egypt

4. Physics Department, College of Science and Humanities Studies Prince Sattam bin Abdulaziz University AlKharj Saudi Arabia

5. Microbiology and Immunology, Faculty of Pharmacy Arab Academy for Science, Technology and Maritime Transport (AASTMT) El‐Alamein Egypt

6. Bioprocess Development Department, Genetic Engineering and Biotechnology Research Institute City of Scientific Research and Technological Applications (SRTA‐City) New Borg El‑Arab City Alexandria Egypt

Abstract

AbstractThe wide biological activity of the Moringa oleifera represents a potential opportunity for developing selective cancer treatment drugs. The bioactive phytochemicals in Moringa seed extract (MSE) indicated large numbers of phytochemicals (21 compounds) with dominant abundance for cycloisolongifolene, 8,9‐dehydro‐9‐vinyl, and chamazulene accounting for 12.7% and 12.19% of the total detected compounds. The MSE showed a potent anticancer effect toward Caco‐2, MDA, and HepG‐2 cells with half‐maximal inhibitory concentration (IC50) values of 9.15 ± 1.18, 4.85 ± 0.11, and 7.36 ± 0.22 µg/mL, respectively, with higher safety (≥31‐folds) toward normal human cells (IC50 of 150.7 ± 11.11 µg/mL). It appears that MSE stimulates selective‐dose‐dependent cell shrinkage, and nuclear condensation in the tumor cells, which finally induces the apoptosis pathway to increase its anticancer action. Additionally, MSE showed a potent capability to stimulate cell cycle arrest in both main checkpoint phases (G0/G1 and G2/M) of cell population growth. The apoptotic death stimulation was confirmed through upregulation of tumor protein p53 (p53) and cyclin‐dependent kinase inhibitor p21 (p21) expression by more than three‐ to sixfold and downregulation of B‐cell lymphoma 2 expression (threefold) in MSE‐treated cells compared to 5‐fluorouracil (5‐FU)‐treated tumor cells. Furthermore, the MSE revealed strong anti‐inflammatory activity with significant antioxidant activity by lowering nitric oxide levels and enhancing the superoxide dismutase activity. On the other hand, the MSE revealed broad‐spectrum antibacterial activity in a dose‐dependent manner against Staphylococcus aureus minimum inhibitory concentration (MIC of 1.25 mg/mL), followed by Salmonella typhimurium (MIC of 1.23 mg/mL), whereas Escherichia coli was the least sensitive to MSE activity (MIC of 22.5 mg/mL) with significant antibiofilm activity against sensitive pathogens.

Publisher

Wiley

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