Clonidine Attenuates Oxidative Stress Induced by H₂O₂ in C6 Glial Cells

Abstract

Oxidative stress plays a critical role in the pathogenesis of neurodegenerative diseases and glioma progression, with glial cells being central to maintaining redox homeostasis. Clonidine, an α2-adrenergic and imidazoline receptor agonist, has demonstrated neuroprotective and antioxidant effects in various experimental models. This study aimed to evaluate the protective effects of clonidine against hydrogen peroxide (H₂O₂)-induced oxidative damage in C6 glial cells. C6 glioma cells were pretreated with clonidine (0.3–4.8 µM) for 1 hour, followed by exposure to 0.5 mM H₂O₂ for 24 hours, and cell viability was assessed using the XTT assay, while total antioxidant status (TAS), total oxidant status (TOS), and superoxide dismutase (SOD) levels were measured using commercial kits and ELISA. H₂O₂ exposure significantly reduced cell viability and antioxidant parameters while increasing oxidative markers; however, clonidine treatment significantly improved cell viability, elevated TAS and SOD levels, and decreased TOS levels compared to the H₂O₂ group, demonstrating its dose-dependent protective effect against oxidative stress. These findings suggest that clonidine mitigates oxidative damage in C6 glial cells, potentially through antioxidant, anti-inflammatory, and imidazoline receptor-mediated mechanisms, and may have therapeutic relevance in conditions characterized by glial oxidative stress, including neurodegenerative diseases and glioma.