ArticleNeurotoxicity research2018
Neuroprotective Effects of Kinetin Against Glutamate-Induced Oxidative Cytotoxicity in HT22 Cells: Involvement of Nrf2 and Heme Oxygenase-1.
Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- A combination of Nrf-2 activator, kinetin and zinc provides neuroprotection through NLRP3-NF-ԟB signaling in traumatic brain injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Kinetin mitigate neurodegenerative damage of Alzheimer induced by beta-amyloid in male rats by antioxidant and antithrombotic effects.Metabolic brain disease · 2026Article
- Antioxidant and Antimelanogenic Activities ofMicroorganisms · 2024Article
- Photoprotective properties of new derivatives of kinetin.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023Article
- Article
- Cytokinins: Wide-Spread Signaling Hormones from Plants to Humans with High Medical Potential.Nutrients · 2022Review
- Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status.Antioxidants (Basel, Switzerland) · 2021Article
- Cytokinin Plant Hormones Have Neuroprotective Activity in In Vitro Models of Parkinson's Disease.Molecules (Basel, Switzerland) · 2021Article
- A Cell-Based High-Throughput Screening Identified Two Compounds that Enhance PINK1-Parkin Signaling.iScience · 2020Article
- Neuroprotective Effect of Natural Alkaloid Fangchinoline Against Oxidative Glutamate Toxicity: Involvement of Keap1-Nrf2 Axis Regulation.Cellular and molecular neurobiology · 2019Article
- New Insights into the Nrf-2/HO-1 Signaling Axis and Its Application in Pediatric Respiratory Diseases.Oxidative medicine and cellular longevity · 2019Review
- N6-Furfuryladenine is protective in Huntington's disease models by signaling huntingtin phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Role of Heme Oxygenases in Cardiovascular Syndromes and Co-morbidities.Current pharmaceutical design · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is considered as one of key factors related to Alzheimer's disease (AD), while kinetin (KT) has been reported to exert anti-oxidative activities as well as neuroprotective effects both in vivo and in vitro. Thus, in this study, the neuroprotective effects of KT against glutamate-induced oxidative toxicity in HT22 cells were investigated. To evaluate the anti-oxidative capabilities of KT itself, several anti-oxidative assays in vitro were conducted. To evaluate the neuroprotective effects of KT, the levels of intracellular reactive oxygen species (ROS) and calcium influx, mitochondrial membrane potential (MMP), and cell death were measured by flow cytometry. Nuclear translocation of apoptosis inducing factor (AIF) and content of intracellular ATP were also determined. In addition, the phosphorylation levels of apoptosis signal-regulating kinase 1 (ASK-1), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinases (p38) were evaluated as well. Besides, nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and the expression of heme oxygenase-1 (HO-1) were also examined to reveal underlying mechanisms. Results showed that KT rescued cell death, and suppressed the accumulation of intracellular ROS and the increase of intracellular calcium influx. In addition, KT maintained normal function of mitochondria and inhibited the phosphorylation of ASK-1, JNK, and p38. KT also promoted nuclear translocation of Nrf2 and enhanced the expression of HO-1 both at protein and mRNA level. Importantly, blockage of Nrf2 almost completely abolished the neuroprotective effects of KT, while blockage of HO-1 expression partly neutralized its neuroprotective effects. Our results indicated that KT can protect HT22 cells from glutamate-induced cell death by activating Nrf2 pathway and inducing expression of HO-1, suggesting KT might be a drug candidate for treatment of AD and other neurodegenerative disorders related to oxidative stress.
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