ArticleJournal of molecular neuroscience : MN2019
Curcumin Alleviates β Amyloid-Induced Neurotoxicity in HT22 Cells via Upregulating SOD2.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Targeting Protein Aggregates with Natural Products: An Optional Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2023Pooled it
- Review
- The Rho kinase signaling pathway participates in tubular mitochondrial oxidative injury and apoptosis in uric acid nephropathy.The Journal of international medical research · 2021Article
- TNFAIP1 Is Upregulated in APP/PS1 Mice and Promotes Apoptosis in SH-SY5Y Cells by Binding to RhoB.Journal of molecular neuroscience : MN · 2021Article
- Intersection between Redox Homeostasis and Autophagy: Valuable Insights into Neurodegeneration.Antioxidants (Basel, Switzerland) · 2021Review
- Involvement of Oxidative Stress and Nerve Growth Factor in Behavioral and Biochemical Deficits of Experimentally Induced Musculoskeletal Pain in Mice: Ameliorative Effects of Heraclin.Journal of molecular neuroscience : MN · 2021Article
- Neuroprotection mediated by natural products and their chemical derivatives.Neural regeneration research · 2020Review
- Mitochondrial DNA and Neurodegeneration: Any Role for Dietary Antioxidants?Antioxidants (Basel, Switzerland) · 2020Review
- Premature synaptic mitochondrial dysfunction in the hippocampus during aging contributes to memory loss.Redox biology · 2020Article
- Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis.Frontiers in aging neuroscience · 2019Article
- SOD2 Mediates Curcumin-Induced Protection against Oxygen-Glucose Deprivation/Reoxygenation Injury in HT22 Cells.Evidence-based complementary and alternative medicine : eCAM · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Curcumin protects neuronal cells exposed to β amyloid (Aβ); the mechanism, however, is still obscure. The aim of this study is to determine whether the type 2 superoxide dismutase (SOD2) mediates curcumin-induced protective effects in Aβ-treated neuronal cells. In this study, the HT22 neuronal cells were exposed to Aβ to imitate neuronal injury in Alzheimer's disease (AD). After 24-h treatment, 10 μM Aβ decreased cell viability and mitochondrial functions, including mitochondrial complex activities and mitochondrial membrane potential (MMP), and also downregulated anti-oxidants SOD2, glutathione (GSH), and catalase (CAT) levels (P < 0.05), meanwhile, increased lactic dehydrogenase (LDH) release, apoptosis level, intracellular reactive oxygen species (ROS) and mitochondrial superoxide accumulation (P < 0.05). And, co-administration of 1 μM curcumin significantly reduced the Aβ-induced cell injury and oxidative damage above (P < 0.05). Downregulating SOD2 by using small interfering RNA (siRNA), however, significantly abolished the curcumin-induced protective and anti-oxidative effects in HT22 cells (P < 0.05); the scramble (SC)-siRNA did not cause marked effects on the curcumin-induced protective effects (P > 0.05). These findings showed that curcumin can alleviate Aβ-induced injury in neuronal cells, and SOD2 protein may mediate the neuroprotective effects.
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Registered trials
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