Moringa oleifera (MO) is an important plant for traditional medicine. The present study aimed to identify the MO active phytochemical compounds for their ability against inflamed macrophages. An ethyl acetate extract fraction of MO was fractionation by flash column chromatography. Human macrophages were stimulated by Lipopolysaccharide and then treated with fractions of MO to examine their anti-inflammatory activity and cellular mechanism. The active fractions were analyzed by liquid chromatography with electrospray ionization quadrupole time-of-flight mass spectrometer (LC-ESI-QTOF-MS). MO treated cells showed a decreased production of pro-inflammatory mediator in response to lipopolysaccharide. This was evident at both mRNA and protein levels. The study revealed that MO suppressed mRNA expression of IL-1, IL-6, TNF-α, PTGS2, NF-κB (P50), and RelA. Furthermore, the extract effectively inhibited the expression of inflammatory mediators, including IL-6, TNF-α, and cyclooxygenase-2. Interestingly, the effect of MO inhibited phosphorylation of IκB-α and the ability to reduce expression of the nuclear factor (NF)-κB p65, suppressing its nuclear translocation. Moreover, LC-ESI-QTOF-MS analysis of the MO active fraction revealed seven compounds, namely 3,4-Methyleneazelaic acid, (2S)-2-phenylmethoxybutane-1,4-diol, (2R)-2-phenylmethoxybutane-1, 4-diol, γ-Diosphenol, 2,2,4,4-Tetramethyl-6-(1-oxobutyl)-1,3,5-cyclohexanetrione, 3-Hydroxy-β-ionone, and Tuberonic acid. Our findings highlight the ability of MO compounds to inhibit inflammation through regulation of the NF-κB pathway.

Squamous cell carcinoma is the most common type of head and neck cancer worldwide. Radiation and chemotherapy are general treatments for patients; however, these remedies can have adverse side effects and tumours develop drug resistance. Effective treatments still require improvement for cancer patients. Here, we investigated the anti-cancer effect of Moringa oleifera (MO) Lam. leaf extracts and their fractions, 3-hydroxy-β-ionone on SCC15 cell line. SCC15 were treated with and without MO leaf extracts and their fractions. MTT assay was used to determine cell viability on SCC15. Cell cycle and apoptosis were evaluated by the Muse™ Cell Analyser. Colony formation and wound closure analysis of SCC15 were performed in 6-well plates. Apoptosis markers were evaluated by immunoblotting. We found that Moringa extracts and 3-HBI significantly inhibited proliferation of SCC15. Moreover, they induced apoptosis and cell cycle arrest at G2/M phase in SCC15 compared to the untreated control. MO extracts and 3-HBI also inhibited colony formation and cell migration of SCC15. Furthermore, we observed the upregulation of cleaved caspase-3 and Bax with downregulation of anti-apoptotic Bcl-2, indicating the induction of cancer cell apoptosis. Our results revealed that MO extracts and 3-HBI provided anti-cancer properties by inhibiting progression and inducing apoptosis of SCC15.

Smokers have high plaque accumulation that initiates gingival inflammation and progresses to periodontitis. Thus, oral hygiene to control microbial plaque formation is an effective method of preventing gingivitis. Medicinal plants such as Moringa oleifera Lam. (MO) and Cyanthillium cinereum (Less.) H. Rob. (CC) have an anti-inflammatory effect that might improve oral health in smokers. This study evaluated the effect of MO leaf and CC extracts using MO lozenges and a combination of MO + CC lozenges on oral inflammation and gingivitis in volunteer smokers. Lozenges consisting of MO and CC extracts were developed and studied in vivo. The results showed that lozenges significantly reduced oral inflammation and gingivitis in volunteers. The gingival index (GI) of group III (MO + CC lozenges) significantly decreased, while the percentage decrease of oral inflammation in group II (MO lozenges) was significantly higher than the other groups. The percentage decrease of GI values in group II (MO lozenges) and group III (MO + CC lozenges) were significantly higher than the placebo group I. Our findings indicated that MO and MO + CC lozenges reduced oral inflammation and gingivitis and showed potential to improve oral health in smokers.

Moringa leaves provide numerous health benefits due to their anti-inflammatory properties. This study presents the first evidence that endothelial cell inflammation can potentially be ameliorated by moringa leaf extract. Here, we established an experimental human blood vessel cell model of inflammation using EA.hy926 cells. TNF-α was added after pre-treating the cells with crude leaf extract from Moringa oleifera Lam., a constituent fraction of the extract, and the bioactive component 3-hydroxy-β-ionone. The extract and the active ingredient significantly decreased the levels of pro-inflammatory mediators such as IL-6, IL-8, and MCP-1; decreased IκB-α and NF-κB p65 phosphorylation; and decreased the expression of VCAM-1, PECAM-1, and ICAM-1, three significant adhesion molecules. Furthermore, they attenuated THP-1 monocyte adhesion to the EA.hy926 monolayer and decreased monocyte transmigration across the monolayer. These findings suggest that 3-hydroxy-β-ionone and moringa leaf extract have anti-inflammatory properties and can be used as therapeutic agents to reduce the progression of diseases involving the inflamed endothelium by decreasing the production of inflammatory cytokines, chemokines, and adhesion molecules. This is promising for conditions such as atherosclerosis and neuroinflammation.

Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype, with limited treatment options and a poor prognosis. Epithelial-to-mesenchymal transition (EMT) plays a critical role in promoting TNBC metastasis. The natural bioactive substance 3-hydroxy-β-ionone (3-HBI), which has been studied in other cancer types, has not yet been examined in TNBC. This study investigates its potential mechanisms in TNBC cells through a combination of computational and experimental approaches, focusing on apoptosis induction and EMT inhibition. Molecular docking and molecular dynamics simulations demonstrated strong and stable binding of 3-HBI to key apoptosis-related proteins (Bcl-2, Bax, caspase-3) and EMT regulators (Smad2, Smad3). In vitro, 3-HBI significantly reduced cell viability in MDA-MB-231, T47D, and MCF7 cells, with IC₅₀ values of 388.40, 185.50, and 113.40 µg/mL, respectively. Moreover, 3-HBI suppressed clonogenic potential, induced apoptosis, and inhibited both migration and invasion. Molecular analysis showed increased expression of Bax, caspase-3, and E-cadherin, and reduced levels of Bcl-2, Smad2, Smad3, and N-cadherin. These findings provide the first mechanistic evidence that 3-HBI exerts anti-TNBC effects by promoting apoptosis and suppressing EMT, highlighting its potential as a promising therapeutic candidate for TNBC treatment.