Methods: VA leaves were extracted using sequential extraction assisted with ultrasound using three different solvents: ethanol, 50% ethanol, and deionized water. The silver nanoparticles were synthesised with VA aqueous extract.
Results: The ethanol extract and VA silver nanoparticles inhibit MCF-7 cell proliferation with an average half-maximal inhibitory concentration (IC50) value of 67µg/mL and 6.11µg/mL, respectively, after 72 hours of treatment. The ethanol extract and VA silver nanoparticles also caused G1 phase cell cycle arrest, induced apoptosis and nuclear fragmentation in MCF-7 cells.
Conclusion: VA ethanol extracts and VA silver nanoparticles decreased the cell viability in MCF-7 cells in a time and dose-dependent manner by inducing apoptosis and causing DNA damage. Further research is needed to elucidate the mechanism of action of VA leaf extracts and VA silver nanoparticles. This study is the first to report on the anticancer activity of VA silver nanoparticles in MCF-7 cells.
METHODS: Methods involved were MTT assay (cytotoxic activity), morphological cells analysis, flow cytometry and cell cycle analysis and western blot.
RESULTS: MTT assay revealed IC50 concentration was 1.61 µg/mL, 3T3-L1 cell lines were used to determine whether AgNps-CN is cytotoxic to normal cells. At the highest concentration (3 µg/mL), no cytotoxic activity has been observed. Flow cytometry assay revealed AgNps-CN caused apoptosis effects towards HSC-4 cell lines with significant changes were observed at G1 phase when compared with untreated cells. Morphological cells analysis revealed that most of the cells exhibit apoptosis characteristics rather than necrosis. Protein study revealed that ratio of Bax/Bcl-2 increased mainly due to down-regulation of Bcl-2 expression.
CONCLUSION: AgNps-CN have shown potential in inhibiting HSC-4 cell lines. IC50 was low compared to few studies involving biosynthesized of silver nanoparticles. Apoptosis effects were shown towards HSC-4 cell lines by the increased in Bax/Bcl-2 protein ratio. Further study such as PCR or in vivo studies are required.
METHODS: Human Wharton's Jelly-derived MSCs were cultured in ascorbic acid supplemented medium for 14 days prior to decellularisation using two methods. 1% SDS/Triton X-100 (ST) or 20 mM ammonia/Triton X-100 (AT). CCs isolated from 4-week-old C57/BL6N mice were cultured on the decellularised MSC matrices, and induced to differentiate into cardiomyocytes in cardiogenic medium for 21 days. Cardiac differentiation was assessed by immunocytochemistry and qPCR. All data were analysed using ANOVA.
RESULTS: In vitro decellularisation using ST method caused matrix delamination from the wells. In contrast, decellularisation using AT improved the matrix retention up to 30% (p
METHODS: The phytochemical fingerprint of C. nutans ethanolic leaf extract was evaluated by LC-MS/MS analysis. We investigated the effects of cisplatin (0-15.23 μg/mL), C. nutans (0-50 μg/mL), and a combination of cisplatin (3.05 μg/mL) and C. nutans (0-50 μg/mL), on cell viability, proliferation, apoptosis, invasion, mRNA expression in cancer stem cells (CD49f, KLF4), and differentiation markers (TUBA1A, KRT18) in TNBC cells. In addition, we also studied the interaction between cisplatin and C. nutans.
RESULTS: Derivatives of fatty acids, carboxylic acid ester, and glycosides, were identified as the major bioactive compounds with potential anticancer properties in C. nutans leaf extract. Reductions in cell viability (0-78%) and proliferation (2-77%), as well as a synergistic anticancer effect, were identified in TNBC cells when treated with a combination of cisplatin and C. nutans. Furthermore, apoptotic induction via increased caspase-3/7 activity (MDA-MB-231: 2.73-fold; MDA-MB-468: 3.53-fold), and a reduction in cell invasion capacity to 36%, were detected in TNBC cells when compared to single cisplatin and C. nutans treatments. At the mRNA level, cisplatin and C. nutans differentially regulated specific genes that are responsible for proliferation and differentiation.
CONCLUSION: Our findings demonstrate that the combination of cisplatin and C. nutans represents a potential treatment for TNBC.
METHODS: AgNP-K 1:1 was synthesized with 1 mM kaempferol, whereas AgNP-K 1:2 with 2 mM kaempferol. The characterization of AgNP-K 1:1 and AgNP-K 1:2 was performed using UV-visible spectroscopy (UV-Vis), Zetasizer, transmission electron microscopy (TEM), scanning electron microscopy-dispersive X-ray spectrometer (SEM-EDX), X-ray diffraction (XRD), and Fourier transform infrared (FTIR) spectroscopy. The antibacterial activities of five samples (AgNP-K 1:1, AgNP-K 1:2, commercial AgNPs, kaempferol, and vancomycin) at different concentrations (1.25, 2.5, 5, and 10 mg/mL) against MRSA were determined via disc diffusion assay (DDA), minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC) assay, and time-kill assay.
RESULTS: The presence of a dark brown colour in the solution indicated the formation of AgNP-K. The UV-visible absorption spectrum of the synthesized AgNP-K exhibited a broad peak at 447 nm. TEM, Zetasizer, and SEM-EDX results showed that the morphology and size of AgNP-K were nearly spherical in shape with 16.963 ± 6.0465 nm in size. XRD analysis confirmed that AgNP-K had a crystalline phase structure, while FTIR showed the absence of (-OH) group, indicating that kaempferol was successfully incorporated with silver. In DDA analysis, AgNP-K showed the largest inhibition zone (16.67 ± 1.19 mm) against MRSA as compared to kaempferol and commercial AgNPs. The MIC and MBC values for AgNP-K against MRSA were 1.25 and 2.50 mg/mL, respectively. The time-kill assay results showed that AgNP-K displayed bacteriostatic activity against MRSA. AgNP-K exhibited better antibacterial activity against MRSA when compared to commercial AgNPs or kaempferol alone.