ArticleEvidence-based complementary and alternative medicine : eCAM2019
SOD2 Mediates Curcumin-Induced Protection against Oxygen-Glucose Deprivation/Reoxygenation Injury in HT22 Cells.
Article in Evidence-based complementary and alternative medicine : eCAM, 2019. 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, 14 citations in OpenAlex.
- Curcumin in vitro Neuroprotective Effects Are Mediated by p62/keap-1/Nrf2 and PI3K/AKT Signaling Pathway and Autophagy Inhibition.Physiological research · 2023Article
- Polyphenols for the Treatment of Ischemic Stroke: New Applications and Insights.Molecules (Basel, Switzerland) · 2022Review
- Mechanisms Underlying Curcumin-Induced Neuroprotection in Cerebral Ischemia.Frontiers in pharmacology · 2022Review
- Protective effects of silibinin on LPS-induced inflammation in human periodontal ligament cells.Frontiers in chemistry · 2022Article
- Selenium-containing protein from selenium-enrichedPharmaceutical biology · 2021Article
- LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3.Human cell · 2021Article
- Curcumin Efficacy in a Serum/Glucose Deprivation-Induced Neuronal PC12 Injury Model.Current molecular pharmacology · 2021Article
- Mitochondrial DNA and Neurodegeneration: Any Role for Dietary Antioxidants?Antioxidants (Basel, Switzerland) · 2020Review
- The Involvement of Mitochondrial Biogenesis in Selenium Reduced Hyperglycemia-Aggravated Cerebral Ischemia Injury.Neurochemical research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Curcumin (Cur) induces neuroprotection against brain ischemic injury; however, the mechanism is still obscure. The aim of this study is to explore the potential neuroprotective mechanism of curcumin against oxygen-glucose deprivation/reoxygenation (OGD/R) injury in HT22 cells and investigate whether type-2 superoxide dismutase (SOD2) is involved in the curcumin-induced protection. In the present study, HT22 neuronal cells were treated with 3 h OGD plus 24 h reoxygenation to mimic ischemia/reperfusion injury. Compared with the normal cultured control group, OGD/R treatment reduced cell viability and SOD2 expression, decreased mitochondrial membrane potential (MMP) and mitochondrial complex I activity, damaged cell morphology, and increased lactic dehydrogenase (LDH) release, cell apoptosis, intracellular reactive oxygen species (ROS), and mitochondrial superoxide (
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Registered trials
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