Journal of the science of food and agriculture · 2026
Ficus carica fruit extract induces mitochondria-mediated apoptosis in C6 glial cells.
СтатьяНазвание и аннотация: Перевод в очереди
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Thangaiyan Radhiga, Dhanabalan Karthik, Veeramani Chinnadurai, Alsaif Mohammed A, Al-Numair Khalid S
Аннотация
BACKGROUND: Ficus carica fruit extract (FCFE) was evaluated for its cytotoxic and apoptotic effects against C6 glial cells. FCFE has been traditionally used for the treatment of neurodegenerative diseases.
METHODS: In this study, cytotoxicity, reactive oxygen species (ROS) generation, and the mitochondrial-mediated apoptotic pathway were investigated.
RESULTS: The cell viability assay confirmed that FCFE treatment pointedly reduced the viability of C6 glial cells in a dose- and time-dependent manner. Excitingly, FCFE exhibited very low toxicity in non-cancerous MCF10A cells, signifying selective activity. Mechanistic studies showed that FCFE treatment in C6 glial cells markedly increased mitochondrial membrane potential and intracellular ROS levels. It induced mitochondrial depolarization and the expression of apoptotic proteins, thereby activating the intrinsic apoptosis pathway and further promoting nuclear condensation. Western blot analysis revealed that FCFE treatment up-regulated pro-apoptotic markers such as Bax, caspase-3, caspase-9, and cytochrome c, and down-regulated the anti-apoptotic marker Bcl-2.
CONCLUSION: These findings conclusively demonstrate that FCFE selectively targets C6 glial cells by inducing mitochondrial-mediated intrinsic apoptosis. Additional preclinical studies using in vivo models are warranted to establish its potent pharmacological properties to make it a promising drug candidate for glioblastoma treatment. © 2026 Society of Chemical Industry.
METHODS: In this study, cytotoxicity, reactive oxygen species (ROS) generation, and the mitochondrial-mediated apoptotic pathway were investigated.
RESULTS: The cell viability assay confirmed that FCFE treatment pointedly reduced the viability of C6 glial cells in a dose- and time-dependent manner. Excitingly, FCFE exhibited very low toxicity in non-cancerous MCF10A cells, signifying selective activity. Mechanistic studies showed that FCFE treatment in C6 glial cells markedly increased mitochondrial membrane potential and intracellular ROS levels. It induced mitochondrial depolarization and the expression of apoptotic proteins, thereby activating the intrinsic apoptosis pathway and further promoting nuclear condensation. Western blot analysis revealed that FCFE treatment up-regulated pro-apoptotic markers such as Bax, caspase-3, caspase-9, and cytochrome c, and down-regulated the anti-apoptotic marker Bcl-2.
CONCLUSION: These findings conclusively demonstrate that FCFE selectively targets C6 glial cells by inducing mitochondrial-mediated intrinsic apoptosis. Additional preclinical studies using in vivo models are warranted to establish its potent pharmacological properties to make it a promising drug candidate for glioblastoma treatment. © 2026 Society of Chemical Industry.