Publications by authors named "Zhisheng Ba"

Alzheimer's disease (AD) is a neurodegenerative disease, which is mainly characterized by the abnormal deposition of β-amyloid peptide (Aβ) and Tau. Since Tau aggregation is more closely associated with synaptic loss, neurodegeneration, and cognitive decline than Aβ, the correlation between Tau and cognitive function in AD has gradually gained attention. The posttranslational modifications (PTMs) of Tau are key factors contributing to its pathological changes, which include phosphorylation, acetylation, ubiquitination, glycosylation, glycation, small ubiquitin-like modifier mediated modification (SUMOylation), methylation, succinylation, etc.

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Objective: To study the protective effect and mechanism of icaritin (ICT) in a SH-SY5Y cells with virus-loaded TAR DNA-binding domain protein 43(TDP-43) by examining the effect of ICT on the expression of autophagy-related proteins in TDP-43-infected SH-SY5Y cells.

Methods: A TDP-43-induced neuronal cell injury model was established by transfecting well-growing SH-SY5Y cells with virus loaded with the TDP-43 gene. The changes in cell viability were detected by the CCK-8 method.

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Background: We assessed whether ICT can alleviate 6-OHDA-induced cell damage inhibition of oxidative stress by evaluating the protective effect of icaritin (ICT) against 6-hydroxydopamine (6-OHDA)-induced MN9D cell damage and further determined the mechanism by which ICT reduces oxidative stress.

Methods: MN9D cells were treated with 6-OHDA, to study the mechanism underlying the neuroprotective effect of ICT. MN9D cell damage was assessed by the CCK-8 assay, flow cytometry was performed to measure the content of reactive oxygen species (ROS) in cells, a superoxide dismutase (SOD) kit was used to evaluate SOD activity, and Western blotting was used to measure the expression of α-synuclein (α-Syn), Tyrosine hydroxylase (TH), nuclear factor erythroid-2 related factor 2 (Nrf2), and heme oxygenase-1 (HO-1).

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Our previous study found that incubating mesenchymal stem cells (MSC) with tanshinone IIA (TIIA) before transplantation could significantly increase the inhibitory effect of MSC on neuroinflammation. Here, we investigated the possible mechanism of this effect. N9 cells and MSC were inoculated at a ratio of 1 : 1 into a Transwell coculture system.

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Objectives: To verify whether mesenchymal stem cells cocultured with tanshinone IIA may ameliorate Alzheimer's disease by inhibiting oxidative stress.

Methods: Sixty male Sprague-Dawley rats were randomly divided into 4 groups named Sham, Aβ25-35, mesenchymal stem cells, and mesenchymal stem cells (tanshinone IIA). The rats were treated according to different groups.

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Background: The aim of this study was to investigate the effect of icaritin (ICT) on TAR DNA-binding protein 43 (TDP-43)-induced neuroblastoma (SH-SY5Y) cell damage and to further explore its underlying mechanisms.

Methods: To investigate the possible mechanism, TDP-43 was used to induce SH-SY5Y cell injury. Cell viability was evaluated by the CCK-8 assay.

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TDP-43 proteinopathy is a kind of neurodegenerative diseases related to the TAR DNA-binding protein of 43-kDa molecular weight (TDP-43). The typical neurodegenerative diseases include amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration (FTLD), Alzheimer's disease (AD), Parkinson's disease (PD) and so on. As the disease process cannot be blocked or slowed down, these patients have poor quality of life and poor prognosis, and bring a huge burden to the family and society.

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Since the discovery of TAR DNA-binding protein 43 (TDP-43) in 1995, our understanding of its role continues to expand as research progresses. In particular, its role in the pathogenesis of Alzheimer's disease (AD) has drawn increasing interest in recent years. TDP-43 may participate in various pathogenic mechanisms underlying AD, such as amyloid β deposition, tau hyperphosphorylation, mitochondrial dysfunction, and neuroinflammation.

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Mesenchymal stem cell transplantation can regulate neuroinflammation and treat Alzheimer's disease (AD), but its effect is attenuated by in vitro expansion. To solve this problem, we used tanshinone IIA (TIIA)-incubated mesenchymal stem cells (MSCs) to treat neuroinflammation caused by amyloid β-protein (Aβ). Here, we demonstrated that behavioral performance was rescued in rats receiving an intracerebroventricular injection of TIIA-incubated MSCs (TIIA-MSCs), and the TIIA-MSCs protected against neurotoxicity in the rat hippocampus by suppressing Aβ-induced neuroinflammation.

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