Protective effects of 20‐hydroxyecdysone on CoCl2‐induced cell injury in PC12 cells
Abstract
20-Hydroxyecdysone, which is found in the rhizomes, roots and the stems of many plants, is an ecdysteroid hormone that regulates molting in insects. We have previously shown that 20-Hydroxyecdysone could alleviate neurological deficits induced by subarachnoid hemorrhage in rabbits. Thus, we hypothesized that 20-Hydroxyecdysone might protect neurons against hypoxic-ischemic injury. In present study, the effects of 20-Hydroxyecdysone on cobalt chloride (CoCl(2))-induced cellular injury in PC12 cells was investigated. The incubation of PC12 cells with CoCl(2) reduced the cell viability, increased the rate of apoptosis. However, when cells were treated with 20-Hydroxyecdysone before or after CoCl(2) exposure, the CoCl(2)-induced cellular injuries were significantly ameliorated. In addition, 20-Hydroxyecdysone dramatically reduced the CoCl(2)-induced production of reactive oxygen species (ROS), decreased the depolarization of the mitochondrial membrane, inhibited the release of cytochrome c into the cytosol and increased the Bax/Bcl-2 ratio. Furthermore, 20-Hydroxyecdysone eliminated the CoCl(2)-induced activation of caspase-3. Taken together, these results indicate that 20-Hydroxyecdysone may protect PC12 cells against CoCl(2)-induced cell injury by inhibiting ROS production and modulating components of the mitochondrial apoptosis pathway. Based on our results, 20-Hydroxyecdysone may be a potential candidate for intervention in hypoxic-ischemic brain injuries such as stroke.
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20E helped recovery of PC12 cells after CoCl2-induced injury, including reduction of reactive oxygen species, a decrease in depolarization of the mitochondrial membrane, and the release of cytochrome C from mitochondria.
“Moreover, 20E helped the recovery of PC12 cells after CoCl2-induced injury, including reduction of reactive oxygen species, a decrease in depolarization of the mitochondrial membrane, and the release of cytochrome C from mitochondria.”
From Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound? (2025) · cites this paper as [45]
The Bcl2/Bax ratio was elevated, and caspase 3 activity was abolished in PC12 cells after CoCl2 injury.
“In line with this, the Bcl2/Bax ratio was elevated, and caspase 3 activity was abolished.”
From Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound? (2025) · cites this paper as [45]
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- Authors
- Hu, J., Zhao, T. Z., Chu, W. H., Luo, C. X., Tang, W. H., Yi, L., & Feng, H.
- Affiliations
- Army Medical University (CN)
- Tang Du Hospital (CN)
- Corresponding author
- Feng, H.
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2010-11-29
- Volume
- 111
- Issue
- 6
- Pages
- 1512-1521
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- OpenAlex
- W2003686605
- Cited by
- 26
- References
- 51
- Citations by year
- 2025: 1 · 2023: 2 · 2022: 2 · 2021: 1 · 2020: 2 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 4 · 2014: 3 · 2013: 2 · 2012: 2
- FWCI
- 0.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cellular Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
- Keywords
- 20-hydroxyecdysone, ecdysteroids, cobalt chloride, hypoxia-ischemia, PC12 cells, neuronal injury, apoptosis, reactive oxygen species, mitochondrial depolarization, cytochrome c release, Bax/Bcl-2 ratio, caspase-3, neuroprotection, stroke
- MeSH terms
- Animals, Cell Survival, Cobalt, Ecdysterone, Enzyme Activation, Flow Cytometry, Blotting, Western, PC12 Cells, Apoptosis, Reactive Oxygen Species, In Situ Nick-End Labeling, Cytochromes c, Rats, Membrane Potential, Mitochondrial, Caspase 3
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