ArticleIranian journal of basic medical sciences2019
Celecoxib, indomethacin, and ibuprofen prevent 6-hydroxydopamine-induced PC12 cell death through the inhibition of NFκB and SAPK/JNK pathways.
Article in Iranian journal of basic medical sciences, 2019. 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, 17 citations in OpenAlex.
- Repurposing celecoxib as adjuvant therapy in patients with Parkinsonian disease: a new therapeutic dawn: randomized controlled pilot study.Inflammopharmacology · 2024Trial
- The Effects of Palmitoylethanolamide or Ibuprofen on the Abundance Profile and Synthesis Rate of Proteins in C2C12 Skeletal Myotubes.FASEB bioAdvances · 2026Article
- Neuroprotection in Parkinson Disease.Neurology and therapy · 2025Review
- Differentiation and regulation of CD4Cellular and molecular life sciences : CMLS · 2024Review
- Identifying Dental Pulp Stem Cell as a Novel Therapeutic trategy for Digestive Diseases.Current stem cell research & therapy · 2024Review
- Versatile Platinum(IV) Prodrugs of Naproxen and Acemetacin as Chemo-Anti-Inflammatory Agents.Cancers · 2023Article
- Neobaicalein, a flavonoid from theIranian journal of basic medical sciences · 2023Article
- Osthole attenuated cytotoxicity induced by 6-OHDA in SH-SY5Y cells through inhibition of JAK/STAT and MAPK pathways.Iranian journal of basic medical sciences · 2023Article
- Neuroinflammation in Parkinson's Disease and its Treatment Opportunities.Balkan medical journal · 2022Article
- Suppressive effects of dental pulp stem cells and its conditioned medium on development and migration of colorectal cancer cells through MAPKinase pathways.Iranian journal of basic medical sciences · 2021Article
- Novel Applications of NSAIDs: Insight and Future Perspectives in Cardiovascular, Neurodegenerative, Diabetes and Cancer Disease Therapy.International journal of molecular sciences · 2021Review
- Combatting Nitrosative Stress and Inflammation with Novel Substituted Triazinoindole Inhibitors of Aldose Reductase in PC12 Cells Exposed to 6-Hydroxydopamine Plus High Glucose.Neurotoxicity research · 2021Article
- Neuroinflammatory responses in Parkinson's disease: relevance of Ibuprofen in therapeutics.Inflammopharmacology · 2021Review
- Protective effects of Cinnamomum verum, Cinnamomum cassia and cinnamaldehyde against 6-OHDA-induced apoptosis in PC12 cells.Molecular biology reports · 2020Article
- Protective effects of vitamin K2 on 6-OHDA-induced apoptosis in PC12 cells through modulation bax and caspase-3 activation.Molecular biology reports · 2019Article
- Pharmacological Targeting of Microglial Activation: New Therapeutic Approach.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe possible action of nonsteroidal anti-inflammatory drugs (NSAIDs) in the reduction of reactive oxygen species (ROS) and also as anti-apoptotic agents may suggest them as putative agents for the treatment of neurodegenerative diseases. This study was designed to explore some pathways alterations induced by NSAIDs following 6-hydroxydopamine (6-OHDA)-induced cell death in PC12 cells as an in vitro model of Parkinson's disease (PD) and to compare the effects of celecoxib, indomethacin and ibuprofen. MATERIALS AND
methodsThe cell viability, ROS content, glutathione (GSH) level, and apoptosis were measured using resazurin, dichlorofluorescein diacetate (DCFH-DA), 5,5'-dithiobis-2-nitrobenzoic acid (DTNB), propidium iodide (PI) and flowcytometry, real-time PCR and western blot.
resultsBased on the results, pretreatment with celecoxib, indomethacin and ibuprofen for 24 hr significantly induced concentration and time-dependent protection against 6-OHDA-induced PC12 cell death. Cell viability (
conclusionIt is suggested that NFκB and SAPK/JNK pathways have an important role in 6-OHDA-induced cell injury. Overall, it seems that pretreatment with NSAIDs protect dopaminergic cells and may have the potential to slow the progression of PD.
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Registered trials
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