Baicalin Attenuated Aβ1-42-Induced Apoptosis in SH-SY5Y Cells by Inhibiting the Ras-ERK Signaling Pathway

Abstract

Alzheimer’s disease (AD) is a serious neurodegenerative disease. It is widely believed that the accumulation of amyloid beta (Aβ) in neurons around neurofibrillary plaques is the main pathological characteristic of AD; however, the molecular mechanism underlying these pathological changes is not clear. Baicalin is a flavonoid extracted from the dry root of Scutellaria baicalensis Georgi. Studies have shown that baicalin exerts excellent anti-inflammatory and neuroprotective effects. In this study, an AD cell model was established by exposing SH-SY5Y cells to Aβ1-42 and treating them with baicalin. Cell survival, cell cycle progression, and apoptosis were measured by MTT, flow cytometry, and immunofluorescence assays, respectively. The expression levels of Ras, ERK/ERK phosphorylation (p-ERK), and cyclin D1 were measured by Western blotting. In addition, whether the MEK activator could reverse the regulatory effect of baicalin on Ras-ERK signaling was investigated using Western blotting. We found that baicalin improved the survival, promoted the proliferation, and inhibited the apoptosis of SH-SY5Y cells after Aβ1-42 treatment. Baicalin also ameliorated Aβ1-42-induced cell cycle arrest at the S phase and induced apoptosis. Furthermore, baicalin inhibited the levels of Ras, p-ERK, and cyclin D1 induced by Aβ, and this effect could be reversed by the MEK activator. Therefore, we suggest that baicalin may regulate neuronal cell cycle progression and apoptosis in Aβ1-42-treated SH-SY5Y cells by inhibiting the Ras-ERK signaling pathway. This study suggested that baicalin might be a useful therapeutic agent for senile dementia, especially AD.

Δ8-THC Protects against Amyloid Beta Toxicity Modulating ER Stress In Vitro: A Transcriptomic Analysis

“…Δ 8 -THC was dissolved in DMSO, diluted in PBS and added at the final concentration in the medium (the final DMSO concentration was <0.1%). Cells were pre-treated with Δ 8 -THC for 24 h. At the end of the pre-treatment, cells were treated with the medium containing 10 µM of Aβ 1-42 for 24 h. This concentration of Aβ 1-42 was chosen based on previous studies showing that it was able to exert cytotoxicity in SH-SY5Y cells [ 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 ]. Control cells and cells pretreated with Δ 8 -THC were incubated with DMEM/F12 medium supplemented with 10% FBS.…”

In vitro Neuroprotective Activity of Vigna radiata L. and Vigna pilosa L. on Amyloid Beta-induced Cytotoxicity

“…Cultured cell lines were maintained at 37°C in an incubator with a humidified 5% CO 2 supply (NBS Eppendorf, Germany). With direct observation of the cells using an inverted phase contrast microscope and the MTT assay method, the vitality of the cells was assessed (Mairuae et al, 2019; Song et al, 2022). Two-day-old confluent monolayers of cells were trypsinized and placed in 96-well tissue culture plates at a density of 5 × 104 cells per well.…”

Baicalin regulates stem cells as a creative point in the treatment of climacteric syndrome

“…Interestingly, Baicalin has the potential to treat AD through inhibiting Ras-ERK signaling pathway and altering the cell cycle composition ratio, thereby preventing apoptosis caused by Aβ accumulation (Song et al, 2022). In addition, Baicalin can improve synaptic plasticity, mitochondrial fragmentation and dysfunction by inhibiting PDE4 activation in a mouse model of AD (Yu et al, 2022).…”

“…As a common form of dementia, AD affects about 50 million people worldwide and is expected to diagnose a new case every 3 s. However, there is currently no effective treatment available ( Liu et al, 2022a ). Interestingly, Baicalin has the potential to treat AD through inhibiting Ras-ERK signaling pathway and altering the cell cycle composition ratio, thereby preventing apoptosis caused by Aβ accumulation ( Song et al, 2022 ). In addition, Baicalin can improve synaptic plasticity, mitochondrial fragmentation and dysfunction by inhibiting PDE4 activation in a mouse model of AD ( Yu et al, 2022 ).…”