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<p>6-Hydroxydopamine (6-OHDA) induces dopaminergic degeneration via oxidative stress. Astaxanthin (AST), a potent antioxidant carotenoid, shows neuroprotective potential, but its effects on human astrocytes (HA) are not fully understood. This study investigated AST’s protective role against 6-OHDA-induced damage in HA cells. HA cells were pretreated with non-toxic AST concentrations (33, 66, 100 µM) before exposure to 6-OHDA (89 µM, IC₅₀). Viability (MTT assay), intracellular ROS, apoptosis, and cell cycle were analyzed by flow cytometry. Bax and Bcl-2 expression were assessed by real-time PCR and ELISA. 6-OHDA reduced viability by ~ 50%, increased ROS, induced G₀/G₁ arrest, and promoted apoptosis/necrosis. AST pretreatment dose-dependently improved viability, reduced ROS, alleviated cell cycle arrest, and decreased apoptotic/necrotic populations. AST also downregulated Bax and upregulated Bcl-2 at mRNA and protein levels, restoring apoptotic balance. AST protects HA cells from 6-OHDA-induced oxidative stress, apoptosis, and cell cycle disruption by modulating ROS and Bax/Bcl-2 pathways. These findings highlight AST’s potential as a neuroprotective agent in Parkinson’s disease.</p> Graphical abstract <p></p>

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Astaxanthin protects human astrocytes (HA) against 6-hydroxydopamine-induced oxidative toxicity

  • 期刊论文

  • 发表日期：

    2026年4月22日

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  • Sarah Hussein Ali Alallo,
  • Zahraa A. Althabet,
  • Heba Akram Mohsin

摘要

6-Hydroxydopamine (6-OHDA) induces dopaminergic degeneration via oxidative stress. Astaxanthin (AST), a potent antioxidant carotenoid, shows neuroprotective potential, but its effects on human astrocytes (HA) are not fully understood. This study investigated AST’s protective role against 6-OHDA-induced damage in HA cells. HA cells were pretreated with non-toxic AST concentrations (33, 66, 100 µM) before exposure to 6-OHDA (89 µM, IC₅₀). Viability (MTT assay), intracellular ROS, apoptosis, and cell cycle were analyzed by flow cytometry. Bax and Bcl-2 expression were assessed by real-time PCR and ELISA. 6-OHDA reduced viability by ~ 50%, increased ROS, induced G₀/G₁ arrest, and promoted apoptosis/necrosis. AST pretreatment dose-dependently improved viability, reduced ROS, alleviated cell cycle arrest, and decreased apoptotic/necrotic populations. AST also downregulated Bax and upregulated Bcl-2 at mRNA and protein levels, restoring apoptotic balance. AST protects HA cells from 6-OHDA-induced oxidative stress, apoptosis, and cell cycle disruption by modulating ROS and Bax/Bcl-2 pathways. These findings highlight AST’s potential as a neuroprotective agent in Parkinson’s disease.

Graphical abstract