RESUMEN

The objective of the present study was to analyze and identify the phytochemical components found in neem leaf extracts using gas chromatography-mass spectrometry (GC-MS) and Fourier-transform infrared spectroscopy (FTIR) methods. The extract samples were acquired using ethyl acetate (EA) and petroleum ether (PE) solvents. Moreover, the extracts were assessed for their antibacterial and antioxidant features. In addition, chitosan nanoparticles (Cs NPs) containing neem extracts were synthesized and evaluated for their potential antibacterial properties, explicitly targeting multi-drug resistant (MDR) bacteria. The neem extracts were analyzed using GC-MS, which identified components such as hydrocarbons, phenolic compounds, terpenoids, alkaloids, and glycosides. Results revealed that the PE extract showed significant antibacterial activity against a range of bacteria. In addition, the PE extract exhibited significant antioxidant activity, exceeding both the EA extract and vitamin C. In addition, both extracts exhibited notable antibiofilm activity, significantly inhibiting the production of biofilm. The Cs NPs, loaded with neem extracts, exhibited significant antibacterial action against multidrug-resistant (MDR) microorganisms. The Cs NPs/EA materials had the greatest zone of inhibition values of 24 ± 2.95 mm against Pseudomonas aeruginosa. Similarly, the Cs NPs/PE materials exhibited a zone of inhibition measurement of 22 ± 3.14 mm against P. aeruginosa. This work highlights the various biochemical components of neem extracts, their strong abilities to combat bacteria and oxidative stress, and the possibility of Cs NPs containing neem extracts as effective treatments for antibiotic-resistant bacterial strains.

Asunto(s)

Antibacterianos , Antioxidantes , Quitosano , Farmacorresistencia Bacteriana Múltiple , Pruebas de Sensibilidad Microbiana , Extractos Vegetales , Quitosano/química , Quitosano/farmacología , Extractos Vegetales/química , Extractos Vegetales/farmacología , Antibacterianos/farmacología , Antibacterianos/química , Farmacorresistencia Bacteriana Múltiple/efectos de los fármacos , Antioxidantes/farmacología , Antioxidantes/química , Nanopartículas/química , Sinergismo Farmacológico , Biopelículas/efectos de los fármacos , Género Justicia/química , Pseudomonas aeruginosa/efectos de los fármacos , Bacterias/efectos de los fármacos

RESUMEN

Background: Atherosclerosis (AS), a major risk factor for stroke and brain tissue destruction, is an inflammatory disease of the blood vessels, and the underlying pathology is inflammation mediated by various chemokines and cytokines. Quercetin, a natural flavonol, is reported to have both anti-inflammatory and antioxidant properties. As such, in the present study, we evaluated the antiatherogenic effects of quercetin in a human THP-1 cell line in vitro and also the signaling mechanisms using in silico analysis. Materials and Methods: THP-1 macrophages exposed to different concentrations of quercetin (5-100 µM for 24 h) were tested for cytotoxicity. Real-time gene expression assay for intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) was carried out following treatment with quercetin at 15 and 30 µM for 24 h either in the absence or presence of interferon (IFN-γ) for 3 h to induce inflammation. Monocyte migration and cholesterol efflux were also assessed. Results: Quercetin did not exert any cytotoxic effects on THP-1 cells at the various concentrations tested. The gene expression assay showed a significant decrease in ICAM-1 (by 3.05 and 2.70) and MCP-1 (by 22.71 and 27.03), respectively. Quercetin at 15 µM decreased THP-1 monocyte migration by 33% compared to the MCP-1-treated cells. It also increased cholesterol efflux significantly by1.64-fold and 1.60-fold either alone or in combination with IFN-γ, respectively. Ingenuity Pathway Analysis of the molecular interactions of quercetin identified canonical pathways directly related to lipid uptake and cholesterol efflux. Furthermore, CD36, SR-A, and LXR-α also demonstrated significant increases by 72.16-, 149.10-, and 29.68-fold, respectively. Conclusion: Our results from both in vitro and in silico studies identified that quercetin inhibited the THP-1 monocyte migration, MCP-1, and ICAM-1 and increased cholesterol efflux probably mediated via the LXR/RXR signaling pathway. Therefore, quercetin will help prevent cell infiltration in atherosclerotic plaques and reduce the risk of stroke or brain destruction.