Schisandrin A Alleviates Inflammation and Oxidative Stress in Aβ25−35-Induced Alzheimer's Disease in Vitro Model

• Siting Jia ^[1] ; Huibo Guan ^[2] ; Shujuan Zhang ^[1] ; Quan Li ^[2]
  1. [1] First Affiliated Hospital of Heilongjiang University of Chinese Medicine

     First Affiliated Hospital of Heilongjiang University of Chinese Medicine

     China

     
  2. [2] Heilongjiang University of Chinese Medicine

     Heilongjiang University of Chinese Medicine

     China

     
• Localización: Actas españolas de psiquiatría, ISSN 1139-9287, Vol. 52, Nº. 5, 2024, págs. 724-732
• Idioma: inglés
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• Resumen

  • Background: Schisandra extract has therapeutic and preventive effects on Alzheimer's disease (AD). Therefore, this study evaluated the anti-AD potential of Schisandrin A (SCH A) using an in vitro cell model.

    Methods: SH-SY5Y and SK-N-SH cells were treated with 20 µM amyloid β-protein (Aβ)25−35. The Aβ25−35-induced cells were then exposed to different concentrations of SCH A (1, 5, 10, 15 µg/mL). Moreover, to further explore the role of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway in the anti-AD effects of SHC A, SH-SY5Y cells were treated with SCH A following incubation with ERK activator LM22B-10. The impact of SCH A on cell viability and apoptosis was evaluated using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and flow cytometry. Furthermore, the oxidative stress markers and inflammatory cytokine levels were also assessed. The reactive oxygen species (ROS) levels were examined using 2′,7′-Dichlorodihydrofluorescein Diacetate (DCFH-DA) method. Finally, Western blot analysis was employed to evaluate the phospho-ERK1/2 (p-ERK1/2) and ERK1/2.

    Results: We observed that SCH A treatment (5, 10, 15 µg/mL) substantially increased the cell viability (p < 0.05), and reduced the apoptosis rate (10 and 15 µg/mL) in SH-SY5Y and SK-N-SH cells (p < 0.05). SCH A significantly ameliorated oxidative stress and reduced inflammatory cytokine levels in Aβ25−35-induced cells (p < 0.05). Furthermore, SCH A up-regulated the p-ERK1/2 to ERK1/2 ratio in Aβ25−35-induced cells. However, LM22B-10 treatment was found to exacerbate this effect of SCH A (p < 0.05).

    Conclusion: SCH A reduces the Aβ25−35-induced inflammatory response and oxidative stress in SH-SY5Y and SK-N-SH cells, and the activation of the ERK/MAPK signaling pathway was related to its potential mechanism.