» Articles » PMID: 39403912

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

Overview
Specialty Psychiatry
Date 2024 Oct 15
PMID 39403912
Authors
Affiliations
Soon will be listed here.
Abstract

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.

References
1.
Cai N, Geng Q, Jiang Y, Zhu W, Yang R, Zhang B . Schisandrin A and B affect the proliferation and differentiation of neural stem cells. J Chem Neuroanat. 2021; 119:102058. DOI: 10.1016/j.jchemneu.2021.102058. View

2.
Chu B, Li M, Cao X, Li R, Jin S, Yang H . IRE1α-XBP1 Affects the Mitochondrial Function of Aβ25-35-Treated SH-SY5Y Cells by Regulating Mitochondria-Associated Endoplasmic Reticulum Membranes. Front Cell Neurosci. 2021; 15:614556. PMC: 8027129. DOI: 10.3389/fncel.2021.614556. View

3.
Zong W, Gouda M, Cai E, Wang R, Xu W, Wu Y . The Antioxidant Phytochemical Schisandrin A Promotes Neural Cell Proliferation and Differentiation after Ischemic Brain Injury. Molecules. 2021; 26(24). PMC: 8706049. DOI: 10.3390/molecules26247466. View

4.
Zhang N, Xu H, Wang Y, Yao Y, Liu G, Lei X . Protective mechanism of kaempferol against Aβ-mediated apoptosis of pheochromocytoma (PC-12) cells through the ER/ERK/MAPK signalling pathway. Arch Med Sci. 2021; 17(2):406-416. PMC: 7959041. DOI: 10.5114/aoms.2020.98199. View

5.
Zhang G, Pare R, Chin K, Qian Y . Tβ4 ameliorates oxidative damage and apoptosis through ERK/MAPK and 5-HT1A signaling pathway in Aβ insulted SH-SY5Y cells. Life Sci. 2021; :120178. DOI: 10.1016/j.lfs.2021.120178. View