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Transcriptomic characterization of human primary prostate stromal cells upon exposure to chemotherapy and treatment by a natural flavonoid apigenin

ABSTRACT: Senescent cells accumulate in a wide variety of solid tissues of mammalian species with advancing age, functionally promoting chronic inflammation and causing age-related diseases. Apigenin is one of the most abundant flavonoids in fruits and vegetables of human diet with several demonstrated health benefits. The aim of the present study is to investigate the influence of apigenin, the natural phytochemical agent with antioxidant, anti-inflammatory and anticancer properties reported by former studies, on human primary stromal cells induced senescent in vitro by a genotoxic agent frequently used in clinical oncology. We mainly focused on the capacity of apigenin in controlling the expression of a full spectrum senescence-associated secretory phenotype (SASP), one of the major hallmarks of senescent cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE273159 | GEO | 2025/06/04

REPOSITORIES: GEO

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Project description:Age is the primary risk factor for many chronic diseases and cognitive decline during brain aging may increase dementia risk. Hallmarks of brain aging including neuronal dysfunction and glial contribute to reduced cognitive function, and there is a persistent lack of effective treatments. Bioactive plant compounds called “nutraceuticals” can target age-related cellular processes and may protect cognitive function. Apigenin is a flavone found in plants such as chamomile and can inhibit hallmarks of aging such as cellular senescence, mitochondrial dysfunction, and impaired proteostasis. However, the underlying mechanisms of apigenin in the brain are not fully understood. Here, we characterized brain transcriptome changes in young and old mice given apigenin in drinking water and examined potential mechanisms in human astrocytes. Consistent with previous studies, we observed improved novel object recognition in old mice treated with apigenin versus old controls. Transcriptome analyses in old controls found differentially expressed genes related to immune responses, inflammation, and cytokine regulation versus young. Fewer differences were observed in old apigenin-treated versus old controls, but these changes were related to development, behavior, and antiviral responses. The majority of upregulated genes in old mice were downregulated with apigenin treatment and associated with immune responses. Similarly, the genes that were reduced with aging, but increased in old apigenin-treated mice were related to pathways important for neurological function/disease, cellular maintenance, and homeostatic signaling. We also found that glial cells drove the majority of the transcriptome differences with aging and apigenin-treatment. To explore the mechanism of action for apigenin in glial cells, we treated replicatively aged astrocytes with apigenin and observed reduced markers of inflammation and cellular senescence. Collectively, our data support the role of apigenin as a protector of cognitive and neuronal function protectant through the suppression of neuroinflammatory genes and proteins and may be especially important in non-neuronal cells.

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Transcriptomic characterization of human primary prostate stromal cells upon exposure to chemotherapy and treatment by a natural flavonoid apigenin

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