ArticleCNS neuroscience & therapeutics2014
Sunitinib produces neuroprotective effect via inhibiting nitric oxide overproduction.
Article in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Optimizing the Sunitinib for cardio-toxicity and thyro-toxicity by scaffold hopping approach.In silico pharmacology · 2022Article
- The Double-Faced Role of Nitric Oxide and Reactive Oxygen Species in Solid Tumors.Antioxidants (Basel, Switzerland) · 2020Review
- Edaravone at high concentrations attenuates cognitive dysfunctions induced by abdominal surgery under general anesthesia in aged mice.Metabolic brain disease · 2020Article
- Article
- Tacrine(10)-Hupyridone Prevents Post-operative Cognitive Dysfunction via the Activation of BDNF Pathway and the Inhibition of AChE in Aged Mice.Frontiers in cellular neuroscience · 2018Article
- 5-Hydroxycyclopenicillone Inhibits β-Amyloid Oligomerization and Produces Anti-β-Amyloid Neuroprotective Effects In Vitro.Molecules (Basel, Switzerland) · 2017Article
- 5-Hydroxycyclopenicillone, a New β-Amyloid Fibrillization Inhibitor from a Sponge-Derived Fungus Trichoderma sp. HPQJ-34.Marine drugs · 2017Article
- Curcumin attenuates surgery-induced cognitive dysfunction in aged mice.Metabolic brain disease · 2017Article
- Indirubin-3-Oxime Prevents HCellular and molecular neurobiology · 2017Article
- Neuroprotective Effects and Mechanisms of Action of Multifunctional Agents Targeting Free Radicals, Monoamine Oxidase B and Cholinesterase in Parkinson's Disease Model.Journal of molecular neuroscience : MN · 2017Article
- Fucoxanthin, a Marine Carotenoid, AttenuatesOxidative medicine and cellular longevity · 2017Article
- Fucoxanthin prevents HFood & nutrition research · 2017Article
- Reactive Oxygen Species-Mediated Mechanisms of Action of Targeted Cancer Therapy.Oxidative medicine and cellular longevity · 2017Review
- Does angiogenesis play a role in the establishment of mesial temporal lobe epilepsy?International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2016Article
- Indirubin-3-Oxime Effectively Prevents 6OHDA-Induced Neurotoxicity in PC12 Cells via Activating MEF2D Through the Inhibition of GSK3β.Journal of molecular neuroscience : MN · 2015Article
- Sunitinib impedes brain tumor progression and reduces tumor-induced neurodegeneration in the microenvironment.Cancer science · 2015Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSunitinib is an inhibitor of the multiple receptor tyrosine kinases (RTKs) for cancer therapy. Some sunitinib analogues could prevent neuronal death induced by various neurotoxins. However, the neuroprotective effects of sunitinib have not been reported.
methodsCerebellar granule neurons (CGNs) and SH-SY5Y cells were exposed to low-potassium and MPP(+) challenges, respectively. MTT assay, FDA/PI staining, Hoechst staining, DAF-FM, colorimetric nitric oxide synthase (NOS) activity assay, and Western blotting were applied to detect cell viability, NO production, NOS activity, and neuronal NOS (nNOS) expression. Short hairpin RNA was used to decrease nNOS expression. In vitro NOS enzyme activity assay was used to determine the direct inhibition of nNOS by sunitinib.
resultsSunitinib prevented low-potassium-induced neuronal apoptosis in CGNs and MPP(+) -induced neuronal death in SH-SY5Y cells. However, PTK787, another RTK inhibitor, failed to decrease neurotoxicity in the same models. Sunitinib reversed the increase in NO levels, NOS activity, and nNOS expression induced by low potassium or MPP(+) . Knockdown of nNOS expression partially abolished the neuroprotective effects of sunitinib. Moreover, sunitinib directly inhibited nNOS enzyme activity.
conclusionsSunitinib exerts its neuroprotective effects by inhibiting NO overproduction, possibly via the inhibition of nNOS activity and the decrease in nNOS expression.
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