ArticleBMC complementary and alternative medicine2016
Neuroprotective effects of Paeonia Lactiflora extract against cell death of dopaminergic SH-SY5Y cells is mediated by epigenetic modulation.
Article in BMC complementary and alternative medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- ZPT01, a herbal formula of Zingiberis Rhizoma, Paeoniae Radix and Tribuli Fructus, protects dopaminergic neurons and suppresses neuroinflammation in a Parkinson's disease model.Molecular biology reports · 2026Article
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2-driven pediatric acute megakaryoblastic leukemia.Genes & diseases · 2026Article
- Paeony root prevents 6-hydroxydopamine-induced neurotoxicity by regulating autophagic dysfunction via AKT signaling in Parkinson's disease models.Metabolic brain disease · 2025Article
- Neuroprotective Effects of Asiatic Acid on Autophagy and Mitochondrial Integrity in a Parkinson's Disease Cellular Model.Journal of experimental pharmacology · 2025Article
- The Genus Paeonia: A Review of the Targeted Signaling Pathways and Underlying Mechanisms of Pharmacological and Clinical Properties.Current drug discovery technologies · 2025Review
- Effects of Histone Modification in Major Depressive Disorder.Current neuropharmacology · 2022Review
- Pharmacological Modulation of Nrf2/HO-1 Signaling Pathway as a Therapeutic Target of Parkinson's Disease.Frontiers in pharmacology · 2021Review
- Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Paeonia lactiflora extract (PLE) has been reported to have neuroprotective effect against neurodegeneration that are induced by cellular stress such as oxidative stress. Its underlying mechanisms, however, remain unclear. In latest decades, emerging evidence has suggested that epigenetic mechanisms play a key role in gene regulation in response to the cellular stress. We investigated whether epigenetic modulation was involved in neuronal cell death by the neurotoxicant, 1-Methyl-4-phenylpyridinium (MPP(+)), and the neuroprotective effect of PLE.
methodsDifferentiated SH-SY5Y, which is a well-established dopaminergic cell line model, was treated with 0 ~ 200 μg/ml PLE for 4 h prior to MPP(+) treatment. The effect of PLE on cell viability was determined by MTT assays. Gene expression levels of oxidative stress responsive genes, such as Heme oxygenase 1 (HMOX1), and histone modifiers, such as histone acetyltransferases (HATs) and deacetylases (HDACs) were measured by quantitative RT PCR. In order to investigate the changes in epigenetic modifications, the acetylated lysine 9 (H3K9ac) and lysine 27 (H3K27ac) of Histone H3 were measured by western blot using histones extracted from the cells.
resultsMPP(+)-induced cell death in SH-SY5Y cells was significantly reduced by PLE pretreatment in a dose-dependent manner, indicating the potent neuroprotective effects of PLE. It was accompanied by induced expression of HMOX1. MPP(+) treatment increased the expression of HATs and consistently increased H3K9ac and H3K27ac of Histone H3. PLE pretreatment impeded the changes in H3K9ac and H3K27ac, coincided with increased expression of HDAC5 without changes in HAT expression.
conclusionsThe results suggested that MPP(+)-induced cell death in the dopaminergic SH-SY5Y cells was related with transcriptional induction of HATs and increased histone H3 acetylation and that PLE might prevent the cells from MPP(+)-induced cell death via tempering histone H3 acetylation.
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