Protective effects of Chinese propolis and its component, chrysin, against neuronal cell death via inhibition of mitochondrial apoptosis pathway in SH-SY5Y cells
Abstract
Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of neurodegenerative and ischemic disorders. The purpose of this study was to evaluate the effects of Chinese propolis and its constituents [chrysin, galangin, pinocembrin, caffeic acid, and caffeic acid phenethyl ester (CAPE)] against tunicamycin-induced neuronal cell death in SH-SY5Y cells. Both Chinese propolis and chrysin concentration-dependently inhibited such cell death, the tunicamycin-induced activation of caspase-3, and the effects of tunicamycin on mitochondria [release of cytochrome c into the cytosol and disruption of the mitochondrial membrane potential (DeltaPsim)]. Furthermore, Chinese propolis and chrysin each inhibited staurosporine-induced cell death. These findings indicate that the inhibitory effects of Chinese propolis against neuronal cell death induced by ER stress or staurosporine may be exerted primarily by chrysin. Moreover, the mechanism underlying the protective effects may, at least partly, involve inhibitions of caspase-3 activity and the mitochondrial apoptotic pathway.
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The human neuroblastoma SH-SY5Y is among the most used cell lines, a subclone of the parental neuronal line SK-N-SH, which originated in 1970 from a biopsy metastatic tumor.
“The human neuroblastoma SH-SY5Y is among the most used cell lines [131,136,137,138,139,140,141,142], a subclone of a parental neuronal line SK-N-SH, which originated in 1970 from a biopsy metastatic tumor.”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [136]
Chinese propolis components inhibited tunicamycin-induced neuronal death in SH-SY5Y cells and decreased induced caspase 3 activation and mitochondrial membrane potential disruption.
“The authors reported the inhibition of neuronal death, and that propolis decreased the induced activation of caspase 3 and the effects on mitochondrial membrane potential disruption [136].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [136]
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- Authors
- Izuta, H., Shimazawa, M., Tazawa, S., Araki, Y., Mishima, S., & Hara, H.
- Affiliations
- Gifu Pharmaceutical University (JP)
- Corresponding author
- Hara, Hideaki
- Venue
- Journal of Agricultural and Food Chemistry
- Publisher
- American Chemical Society (ACS)
- Published
- 2008-09-12
- Volume
- 56
- Issue
- 19
- Pages
- 8944-8953
- ISSN
- 0021-8561 (ISSN-L)
- 1520-5118
- OpenAlex
- W2070668428
- Cited by
- 93
- References
- 31
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 2 · 2021: 8 · 2020: 11 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 10 · 2015: 6 · 2014: 4 · 2013: 3 · 2012: 5
- FWCI
- 6.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Agricultural and Food Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Agricultural and Biological Sciences › Insect Science › Bee Products Chemical Analysis
- Health Sciences › Medicine › Pharmacology › Flavonoids in Medical Research
- Health Sciences › Medicine › Pharmacology › Healthcare and Venom Research
- Keywords
- Chinese propolis, chrysin, neuronal cell death, endoplasmic reticulum stress, mitochondrial apoptosis, caspase-3, cytochrome c release, mitochondrial membrane potential, tunicamycin, staurosporine, SH-SY5Y cells, neuroprotection, caffeic acid phenethyl ester, galangin, pinocembrin, caffeic acid
- MeSH terms
- Endoplasmic Reticulum, Enzyme Activation, Flavonoids, Humans, Mitochondria, Neuroblastoma, Neurons, Propolis, Tunicamycin, Apoptosis, Staurosporine, Cell Line, Tumor, Membrane Potential, Mitochondrial, Caspase 3
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