ArticleCellular and molecular neurobiology2014
Protective effect of paeoniflorin on Aβ25-35-induced SH-SY5Y cell injury by preventing mitochondrial dysfunction.
Article in Cellular and molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 95 citations in OpenAlex.
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- 11,12-Diacetyl-carnosol Protects SH-SY5Y Cells from Hydrogen Peroxide Damage through the Nrf2/HO-1 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- A review for the pharmacological effects of paeoniflorin in the nervous system.Frontiers in pharmacology · 2022Review
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- Carnosic acid depends on glutathione to promote mitochondrial protection in methylglyoxal-exposed SH-SY5Y cells.Metabolic brain disease · 2021Article
- Mitochondrial Protection and Anti-inflammatory Effects Induced by Emodin in the Human Neuroblastoma SH-SY5Y Cells Exposed to Hydrogen Peroxide: Involvement of the AMPK/Nrf2 Signaling Pathway.Neurochemical research · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a major neurodegenerative brain disorder affecting about 14 million people worldwide. Aβ-induced cell injury is a crucial cause of neuronal loss in AD, thus the suppression of which might be useful for the treatment of this disease. In this study, we aimed to evaluate the effect of paeoniflorin (PF), a monoterpene glycoside isolated from aqueous extract of Radix Paeoniae Alba, on Aβ25-35-induced cytotoxicity in SH-SY5Y cells. The results showed PF could attenuate or restore the viability loss, apoptotic increase, and ROS production induced by Aβ25-35 in SH-SY5Y cells. In addition, PF strikingly inhibited Aβ25-35-induced mitochondrial dysfunction, which includes decreased mitochondrial membrane potential, increased Bax/Bcl-2 ratio, cytochrome c release and activity of caspase-3 and caspase-9. Therefore, our study provided the first experimental evidence that PF could modulate ROS production and apoptotic mitochondrial pathway in model of neuron injury in vitro and which might provide new insights into its application toward Alzheimer's disease therapy.
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