Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2026
The potential of astaxanthin in reducing lithium-induced neuroinflammation: Inhibitory effects on the NF-κB pathway.
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Gelen Volkan, Kara Adem, Kara Hülya, Özkanlar Seçkin, Yakut Seda, Ulucan Aykut, Çalık Fatma
Аннотация
BACKGROUND: Lithium (LIT) can induce neurotoxicity through multiple mechanisms, including oxidative stress, neuroinflammation, and dysregulation of neuronal survival and cell death pathways. Astaxanthin (AST) is a xanthophyll carotenoid with potent antioxidant and anti-inflammatory properties and can scavenge reactive oxygen species. This study aimed to investigate the potential neuroprotective effects of AST against LIT-induced brain injury, with particular emphasis on oxidative stress, neuroinflammation, apoptosis, autophagy, and intracellular survival signaling.
METHODS: Rats were assigned to Control, AST, Li, and AST+Li groups, and the effects of LIT exposure and AST treatment were evaluated after 14 and 28 days. Neuronal damage and microglial responses were evaluated histopathologically. The protein expression levels of Bax, Caspase-3, Bcl-2, LC3, Beclin-1, PI3K, CREB, and NF-κB-p65 were determined. In addition, serum levels of the pro-inflammatory cytokines IL-1β, IFN-γ, and TNF-α were assessed by ELISA, and oxidative stress was evaluated using GSH, MDA, and SOD levels.
RESULTS: LIT exposure induced neuronal damage and increased microglial cell numbers, accompanied by increased oxidative stress and elevated pro-inflammatory cytokine levels. At the molecular level, LIT increased Bax, Caspase-3, LC3, Beclin-1, and NF-κB-p65 expression, reduced Bcl-2 and PI3K expression, and altered CREB expression. AST co-administration partially reversed these molecular alterations. AST treatment attenuated neuronal damage and microglial activation, improved oxidative balance, reduced pro-inflammatory cytokine levels, and favorably regulated apoptosis-, autophagy-, inflammation-, and survival-related proteins. Overall, the neuroprotective effects of AST were more pronounced with the longer treatment period.
CONCLUSION: AST attenuated LIT-induced neurotoxicity by reducing oxidative stress, neuroinflammation, and apoptotic responses while modulating autophagy and neuronal survival signaling. These findings suggest that the neuroprotective effects of AST are associated with suppression of NF-κB-mediated inflammatory responses and regulation of apoptosis-, autophagy-, and PI3K/CREB-associated signaling pathways.
METHODS: Rats were assigned to Control, AST, Li, and AST+Li groups, and the effects of LIT exposure and AST treatment were evaluated after 14 and 28 days. Neuronal damage and microglial responses were evaluated histopathologically. The protein expression levels of Bax, Caspase-3, Bcl-2, LC3, Beclin-1, PI3K, CREB, and NF-κB-p65 were determined. In addition, serum levels of the pro-inflammatory cytokines IL-1β, IFN-γ, and TNF-α were assessed by ELISA, and oxidative stress was evaluated using GSH, MDA, and SOD levels.
RESULTS: LIT exposure induced neuronal damage and increased microglial cell numbers, accompanied by increased oxidative stress and elevated pro-inflammatory cytokine levels. At the molecular level, LIT increased Bax, Caspase-3, LC3, Beclin-1, and NF-κB-p65 expression, reduced Bcl-2 and PI3K expression, and altered CREB expression. AST co-administration partially reversed these molecular alterations. AST treatment attenuated neuronal damage and microglial activation, improved oxidative balance, reduced pro-inflammatory cytokine levels, and favorably regulated apoptosis-, autophagy-, inflammation-, and survival-related proteins. Overall, the neuroprotective effects of AST were more pronounced with the longer treatment period.
CONCLUSION: AST attenuated LIT-induced neurotoxicity by reducing oxidative stress, neuroinflammation, and apoptotic responses while modulating autophagy and neuronal survival signaling. These findings suggest that the neuroprotective effects of AST are associated with suppression of NF-κB-mediated inflammatory responses and regulation of apoptosis-, autophagy-, and PI3K/CREB-associated signaling pathways.