Nanomedicine (London, England) · 2026
Injectable etoposide-loaded dextran nanoparticles for breast cancer treatment: physicochemical characterization, cytotoxicity studies, macrophage activity, and gene expression profiling.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Moni Sivakumar S, Qadri Marwa M, Moshi Jobran M, Hawsawi Yousef M, Alotaibi Shmoukh, Riadi Yassine, Halawi Hatim Ali Asiri, Sultan Muhammad H, Salawi Ahmad, Kameli Nader, Mobarki Ahmed Ali, Kaabi Majed Ahmed, Rehman Zia Ur, Elmobark Mohamed Eltaib, Aljahdali Ieman A, Oraibi Bassem, Shabaj Haneen Mohammed, Jeraiby Mohammed A
Аннотация
AIM: This study aimed to develop and characterize injectable etoposide-loaded dextran sulfate sodium nanoparticles (ETP-DNPs).
METHODS: ETP-DNPs were prepared by ionic gelation and characterized. In vitro drug release was studied for 8 h, cytotoxicity was assessed in MCF-7 breast cancer cells, macrophage activation was analyzed using IL-6 stimulation, and apoptosis-related gene expression (Bax, p53, and BCL-2) was evaluated by qRT-PCR.
RESULTS: ETP-DNPs exhibited excellent electrostatic stability (zeta potential -33.2 ± 8.21 mV), a Z-average size of 13.03 nm, predominant particle size of 9.5 ± 3.14 nm, and a PDI of 0.314. SEM confirmed uniform spherical morphology. DSC revealed endothermic peaks between 133.5-185.2°C and an exothermic peak at 210.9°C, while TGA indicated major degradation at 286.9°C. Raman spectra showed sulfate - glycosidic interactions, and XRD peaks indicated partial crystallinity. Drug loading and encapsulation efficiency were high (83.3% and 84.6%). Drug release reached 73.45% with near zero-order kinetics. MCF-7 viability decreased dose- and time-dependently, and IL-6 assays confirmed M1 activation. ETP-DNP treatment markedly inhibited MCF-7 cell migration in a scratch assay, with minimal wound closure observed up to 48 h compared with untreated controls, indicating reduced migratory potential. In parallel, ETP-DNPs induced apoptosis by significantly upregulating Bax and increasing the Bax/BCL2 ratio, confirming activation of the intrinsic mitochondrial apoptotic pathway.
CONCLUSION: The research findings validate ETP-DNP as a promising nanocarrier system for breast cancer. .
METHODS: ETP-DNPs were prepared by ionic gelation and characterized. In vitro drug release was studied for 8 h, cytotoxicity was assessed in MCF-7 breast cancer cells, macrophage activation was analyzed using IL-6 stimulation, and apoptosis-related gene expression (Bax, p53, and BCL-2) was evaluated by qRT-PCR.
RESULTS: ETP-DNPs exhibited excellent electrostatic stability (zeta potential -33.2 ± 8.21 mV), a Z-average size of 13.03 nm, predominant particle size of 9.5 ± 3.14 nm, and a PDI of 0.314. SEM confirmed uniform spherical morphology. DSC revealed endothermic peaks between 133.5-185.2°C and an exothermic peak at 210.9°C, while TGA indicated major degradation at 286.9°C. Raman spectra showed sulfate - glycosidic interactions, and XRD peaks indicated partial crystallinity. Drug loading and encapsulation efficiency were high (83.3% and 84.6%). Drug release reached 73.45% with near zero-order kinetics. MCF-7 viability decreased dose- and time-dependently, and IL-6 assays confirmed M1 activation. ETP-DNP treatment markedly inhibited MCF-7 cell migration in a scratch assay, with minimal wound closure observed up to 48 h compared with untreated controls, indicating reduced migratory potential. In parallel, ETP-DNPs induced apoptosis by significantly upregulating Bax and increasing the Bax/BCL2 ratio, confirming activation of the intrinsic mitochondrial apoptotic pathway.
CONCLUSION: The research findings validate ETP-DNP as a promising nanocarrier system for breast cancer. .