Modulation of oxidative stress and mitochondrial alteration in IL1β-stimulated human astrocytes: effects of extracts from leaves and rhizomes of Posidonia oceanica (L) Delile

Chronic inflammation is a major risk factor for mitochondrial dysfunction and oxidative stress in the central nervous system (CNS). Astrocytes are highly susceptible to pro-inflammatory cytokines, such as IL-1β, which can lead to altered redox homeostasis and mitochondrial dysfunction [1]. In this study, primary cultured human astrocytes were exposed to IL-1β to induce an inflammatory state and subsequently treated with extracts obtained from either green leaves or rhizomes of the marine phanerogam P. oceanica, which are rich in polyphenolic compounds with neuroprotective capabilities [2]. Preliminary data on the same experimental model had revealed a reduction in IL-1β induced-reactive oxygen species levels following treatment with the two extracts [3]. Therefore, this study aimed to further investigate the modulation of oxidative stress and mitochondrial alteration. Fluorescent imaging with Mitosox Red evidenced a partial reduction in superoxide levels following co-treatment with both extracts. In parallel, the analysis of mitochondrial morphology showed that the co-treatments contributed to recover the mitochondrial morphology, although to a restricted degree potentially attributable to the brief analytical timeframe. Ultimately, the analysis of the expression levels of DRP-1, a key regulator of mitochondrial fission, showed a significant downregulation following co-treatment, suggesting the inhibition of the mitochondrial fission process induced by IL-1β. Overall, these preliminary findings suggest that P. oceanica’s extracts may exert a protective effect against inflammation-induced mitochondrial oxidative stress in human astrocytes, thereby endorsing their prospective application as neuroprotective agents in neuroinflammatory pathologies. Further studies are required to assess these impacts across extended duration and to establish if full mitochondrial function integrity can be restablished.