ArticleJournal of molecular neuroscience : MN2014
Pinocembrin protects SH-SY5Y cells against MPP+-induced neurotoxicity through the mitochondrial apoptotic pathway.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Functional Expression of NMDA Receptors in SH-SY5Y Neuroblastoma Cells Following Long-Term RA/BDNF-Induced Differentiation.NeuroSci · 2025Article
- Curcumin protects against MPPMolecular biology reports · 2025Article
- Review
- The Nrf2-HO-1 system and inflammaging.Frontiers in immunology · 2024Review
- Protective Effects of Whey Protein Hydrolysate, Treadmill Exercise, and Their Combination against Scopolamine-Induced Cognitive Deficit in Mice.Foods (Basel, Switzerland) · 2023Article
- The Study of Overexpression of Peroxiredoxin-2 Reduces MPPNeurochemical research · 2023Article
- An In Vitro Evaluation of the Potential Neuroprotective Effects of Intranasal Lipid Nanoparticles Containing Astaxanthin Obtained from Different Sources: Comparative Studies.Pharmaceutics · 2023Article
- Engineered living materials for the conversion of a low-cost food-grade precursor to a high-value flavonoid.Frontiers in bioengineering and biotechnology · 2023Article
- Fiscalin Derivatives as Potential Neuroprotective Agents.Pharmaceutics · 2022Article
- Roles of Heme Oxygenase-1 in Neuroinflammation and Brain Disorders.Antioxidants (Basel, Switzerland) · 2022Review
- Potential Effects of Romanian Propolis Extracts against Pathogen Strains.International journal of environmental research and public health · 2022Article
- Pinocembrin pretreatment counteracts the chlorpyrifos-induced HO-1 downregulation, mitochondrial dysfunction, and inflammation in the SH-SY5Y cells.Metabolic brain disease · 2021Article
- Synthesis of Novel Pinocembrin Amino Acid Derivatives and Their Antiaging Effect onDrug design, development and therapy · 2021Article
- Apitherapy for Age-Related Skeletal Muscle Dysfunction (Sarcopenia): A Review on the Effects of Royal Jelly, Propolis, and Bee Pollen.Foods (Basel, Switzerland) · 2020Review
- Apitherapy for Parkinson's Disease: A Focus on the Effects of Propolis and Royal Jelly.Oxidative medicine and cellular longevity · 2020Review
- Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Evidence on the Health Benefits of Supplemental Propolis.Nutrients · 2019Review
- Advances in Biosynthesis, Pharmacology, and Pharmacokinetics of Pinocembrin, a Promising Natural Small-Molecule Drug.Molecules (Basel, Switzerland) · 2019Review
- Pinocembrin Protects from AGE-Induced Cytotoxicity and Inhibits Non-Enzymatic Glycation in Human Insulin.Cells · 2019Article
- The Nrf2/HO-1 Axis as Targets for Flavanones: Neuroprotection by Pinocembrin, Naringenin, and Eriodictyol.Oxidative medicine and cellular longevity · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pinocembrin (PB), the most abundant flavonoid in propolis, has been proven to have neuroprotective property against neurotoxicity in vivo and in vitro. Our recent study demonstrated the neuroprotective effect of PB against Aβ25-35-induced SH-SY5Y neurotoxicity. However, the mechanism as how PB can induce neuroprotection is not known. In the present study, we demonstrate here that PB abrogates the effects of the neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) which mimics Parkinson's disease (PD) with elevation of intracellular reactive oxygen species (ROS) level and apoptotic death. We found that pretreatment of SH-SY5Y cells with PB significantly reduced the MPP(+)-induced loss of cell viability, the generation of intracellular ROS, apoptotic rate, and the cleavage of caspase-3. PB strikingly inhibited MPP(+)-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio, and the release of cytochrome c. Overall, these results suggest that PB is intimately involved in inhibiting MPP(+)-induced loss of mitochondrial function and induction of apoptosis that contributes toward neuronal survival. These data indicated that PB might provide a valuable therapeutic strategy for the treatment of PD.
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