Trans-cinnamaldehyde Attenuates H₂o₂-induced Cellular Senescence in Human Svgp12 Astroglial Cells

Background Aging is characterized by progressive functional decline driven by oxidative stress, inflammation, and cellular senescence. Astrocytes are particularly vulnerable to oxidative injury, making them a relevant cellular model for investigating aging-related neurodegenerative mechanisms. Trans-cinnamaldehyde (TCA), a major bioactive component of cinnamon, exhibits antioxidant and anti-inflammatory properties; however, its role in astroglial senescence remains poorly understood. Methods Oxidative stress-induced senescence was established in SVGp12 astroglial cells100 µM hydrogen peroxide (H2O2) was used to achieve this. Senescence was confirmed by morphological alterations, reduced cell viability (WST-8 assay), and senescence-associated β-galactosidase (SA-β-gal) staining. Following cytotoxicity screening, TCA was applied at a non-toxic concentration. HIF-1α expression was evaluated by immunocytochemistry (ICC) and semi-quantified using H-score analysis. Levels of KEAP1, TNF-α, IL-1β, IL-6 and NRF2 were measured by ELISA. Results H₂O₂ exposure significantly induced astroglial senescence, increased SA-β-gal positivity, elevated HIF-1α immunoreactivity, and upregulated proinflammatory cytokines and KEAP1/NRF2 signaling. TCA treatment made a big difference in cell viability, reduced the changes to cells that happen as they age, and decreased the expression of HIF-1α. Moreover, TCA markedlyattenuated the H₂O₂-induced increases in IL-6, KEAP1, TNF-α, NRF2 and IL-1β levels. Conclusion TCA effectively mitigates oxidative stress-induced senescence in astroglial cells by reducing HIF-1α expression, inflammatory cytokine production, and redox stress signaling. TCA may be a natural compound that can target astrocyte-associated ageing and neuroinflammation, according to these findings.