ArticleCellular and molecular neurobiology2015
PEG-PEI/siROCK2 Protects Against Aβ42-Induced Neurotoxicity in Primary Neuron Cells for Alzheimer Disease.
Article in Cellular and molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Targeting the FSH/FSHR axis in ovarian cancer: advanced treatment using nanotechnology and immunotherapy.Frontiers in endocrinology · 2024Review
- Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review).International journal of molecular medicine · 2023Review
- Article
- Neuroprotective activity of natural products isolated from Senecio graciliflorus DC against corticosterone-induced impairment in SH-SY5Y cells.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- The Cellular Prion Protein-ROCK Connection: Contribution to Neuronal Homeostasis and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Review
- Neuroprotective Effects of Salidroside in a Mouse Model of Alzheimer's Disease.Cellular and molecular neurobiology · 2020Article
- Induction of p73, Δ133p53, Δ160p53, pAKT lead to neuroprotection via DNA repair by 5-LOX inhibition.Molecular biology reports · 2020Article
- Retro-inverso follicle-stimulating hormone peptide-mediated polyethylenimine complexes for targeted ovarian cancer gene therapy.Drug delivery · 2018Article
- Neuroprotective effects of salidroside through PI3K/Akt pathway activation in Alzheimer's disease models.Drug design, development and therapy · 2016Article
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Authors and funding
8 authors.
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Abstract
Gene therapy that targets the ROCK2 gene has yielded promising results in the treatment of AD. Our previous study indicated that PEG-PEI/siROCK2 could effectively suppress ROCK2 mRNA expression and showed a promising prospect for the treatment of Alzheimer's disease. However, the ability of PEG-PEI/siROCK2 to reduce Aβ-induced cytotoxicity is unknown. To investigate the effect of PEG-PEI/siROCK2 against Aβ42-induced neurotoxicity, primary cultured cortical neurons were pretreated with PEG-PEI/siROCK2 for 24 h and then treated with 5 μM Aβ42 for 24 h. We found that PEG-PEI/siROCK2 increased the cell viability and reduced the number of apoptotic cells induced by Aβ42, as measured using an MTT assay and Annexin V/PI staining. A further study revealed that PEG-PEI/siROCK2 can activate p-Akt, and treatment with the PI3K inhibitor LY294002 attenuated the neuroprotective effects. These results suggest that PEG-PEI/siROCK2 prevents Aβ42-induced neurotoxicity and that the activation of PI3K/Akt pathway is involved in neuroprotection. Taken together, these findings shed light on the role of PEG-PEI/siROCK2 as a potential therapeutic agent for AD.
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