ArticleAmerican journal of translational research2026
Cross-linked (R)-(+)-lipoic acid nanoparticles loaded with silibinin induce apoptosis and autophagy in glioblastoma cells.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo overcome the limitations of poor water solubility and suboptimal tumour-targeting efficiency of silibinin (SF), this study aimed to develop a novel (R)-(+)-lipoic acid (LA)-derived nanocarrier platform to enhance its delivery efficiency and to investigate its antitumor effects and underlying mechanisms in glioblastoma.
methodsSilibinin-loaded (R)-(+)-lipoic acid nanoparticles (SF@LA-NPs) were prepared by a self-assembly approach combined with ultraviolet light-induced crosslinking. Their physicochemical properties, drug encapsulation efficiency, and glutathione (GSH)-responsive release were systematically characterized. Human glioblastoma U87-MG cells were used to evaluate the anti-glioblastoma effects and underlying mechanisms through cytotoxicity assays, intracellular uptake analysis, apoptosis/autophagy analysis, and exploration of the interplay between autophagy and apoptosis.
resultsSF@LA-NPs exhibited uniform particle sizes, high drug encapsulation, and rapid GSH-responsive cargo release. Compared to free SF, SF@LA-NPs markedly enhanced intracellular uptake and cytotoxicity. SF@LA-NPs induced overproduction of reactive oxygen species (ROS), leading to mitochondrial damage and activation of the Caspase-3-dependent apoptosis pathway. Notably, SF@LA-NPs concurrently triggered a protective autophagic response, as indicated by increased LC3-II conversion and reduced p62. In addition, a functional antagonistic relationship was uncovered: pharmacologic inhibition of autophagy enhanced apoptosis and cytotoxicity, while inhibition of apoptosis attenuated cell death and altered autophagic activity.
conclusionSF@LA-NPs developed in this study significantly enhanced the delivery efficiency and antitumor activity of silibinin in glioblastoma cells. Moreover, a dual-mechanism mode of action was elucidated, involving ROS-induced mitochondrial apoptosis and compensatory protective autophagy. These findings provide a promising nano-platform and a theoretical basis for combination therapies targeting apoptosis-autophagy crosstalk in glioblastoma.
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