20-Hydroxyecdysone Protects against Oxidative Stress-Induced Neuronal Injury by Scavenging Free Radicals and Modulating NF-κB and JNK Pathways
Open accessAbstract
Oxidative stress plays an important role in the pathological processes of ischemic brain damage. Many antioxidants have been shown to protect against cerebral ischemia injury by inhibiting oxidative stress both in vitro and in vivo. 20-Hydroxyecdysone (20E), an ecdysteroid hormone, exhibits antioxidative effects. For the work described in this paper, we used an in vitro oxidative damage model and an in vivo ischemic model of middle cerebral artery occlusion (MCAO) to investigate the neuroprotective effects of 20E and the mechanisms related to these effects. Treatment of cells with H(2)O(2) led to neuronal injury, intracellular ROS/RNS generation, mitochondrial membrane potential dissipation, cellular antioxidant potential descent, an increase in malondialdehyde (MDA) and an elevation of intracellular [Ca(2+)], all of which were markedly attenuated by 20E. Inhibition of the activation of the ASK1-MKK4/7-JNK stress signaling pathway and cleaved caspase-3 induced by oxidative stress were involved in the neuroprotection afforded by 20E. In addition, 20E reduced the expression of iNOS protein by inhibition of NF-κB activation. The neuroprotective effect of 20E was also confirmed in vivo. 20E significantly decreased infarct volume and the neurological deficit score, restored antioxidant potential and inhibited the increase in MDA and TUNEL-positive and cleaved caspase-3-positive cells in the cerebral cortex in MCAO rats. Together, these results support that 20E protects against cerebral ischemia injury by inhibiting ROS/RNS production and modulating oxidative stress-induced signal transduction pathways.
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Ecdysterone reduced iNOS expression by inhibiting NFκB activation and inhibited activation of the ASK1-MKK4/7-JNK stress signalling pathway.
“It also reduced iNOS expression by inhibiting NFκB activation and inhibited activation of the ASK1-MKK4/7-JNK stress signalling pathway.”
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 [47]
After occlusion of the cerebral artery, 20E decreased infarct volume and neural deficit score, restored anti-oxidant capacity, decreased malondialdehyde level, and decreased TUNEL-positive cells and cells with cleaved caspase 3 in the cerebral cortex.
“After occlusion of the cerebral artery, 20E decreased the infarct volume and the neural deficit score; furthermore, it restored anti-oxidant capacity, decreased malondialdehyde level, and decreased the number of TUNEL-positive cells and the number of cells with cleaved caspase 3 in the cerebral cortex.”
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 [47]
Ecdysterone attenuated ROS/RNS production, dissipation of mitochondrial membrane potential, descent of anti-oxidant potential, level of malondialdehyde, and intracellular Ca2+ levels in B35 cells.
“Ecdysterone markedly attenuated ROS/RNS production, dissipation of mitochondrial membrane potential, descent of anti-oxidant potential, level of malondialdehyde, and level of intracellular Ca2+ levels.”
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 [47]
20-hydroxyecdysone is able to mediate its neuroprotective effect by activating cellular antioxidant enzymes, inhibiting oxidative stress, and reducing the levels of reactive oxygen species.
“The component 20-hydroxyecdysone is able to mediate its neuroprotective effect by activating cellular antioxidant enzymes, inhibiting oxidative stress, and reducing the levels of reactive oxygen species [40].”
From Anxiolytic and Antioxidant Effect of Phytoecdysteroids and Polyphenols from Chenopodium quinoa on an In Vivo Restraint Stress Model (2022) · cites this paper as [40]
The increase in the activity of SOD revealed 24 h after stress exposure against the background of animal consumption of FFIs suggests that its main components, namely 20-hydroxyecdysone and polyphenols, can act as suppressors and activate the antioxidant defense system.
“The increase in the activity of SOD revealed in our study 24 h after stress exposure against the background of animal consumption of FFIs suggests that its main components, namely 20-hydroxyecdysone and polyphenols, can act as suppressors and activate the antioxidant defense system.”
From Anxiolytic and Antioxidant Effect of Phytoecdysteroids and Polyphenols from Chenopodium quinoa on an In Vivo Restraint Stress Model (2022) · cites this paper as [40]
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- Authors
- Hu, J., Luo, C. X., Chu, W. H., Shan, Y. A., Qian, Z.-M., Zhu, G., Yu, Y. B., & Feng, H.
- Affiliations
- Army Medical University (CN)
- China-Japan Friendship Hospital (CN)
- Corresponding author
- Yu, Yan Bing
- Feng, Hua
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-12-11
- Volume
- 7
- Issue
- 12
- Pages
- e50764
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3519785
- OpenAlex
- W2033637248
- Cited by
- 67
- References
- 63
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 6 · 2023: 5 · 2022: 5 · 2021: 5 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 6 · 2014: 11 · 2013: 2
- FWCI
- 3.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81070929, 304803920)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Keywords
- 20-hydroxyecdysone, ecdysteroids, neuroprotection, cerebral ischemia, oxidative stress, middle cerebral artery occlusion, free radical scavenging, NF-κB, JNK signaling, caspase-3, inducible nitric oxide synthase, malondialdehyde, mitochondrial membrane potential, reactive oxygen species, reactive nitrogen species, infarct size
- MeSH terms
- Animals, Antioxidants, Brain Ischemia, Ecdysterone, Hydrogen Peroxide, Neurons, Signal Transduction, Reperfusion Injury, Free Radical Scavengers, NF-kappa B, Rats, Sprague-Dawley, Apoptosis, Oxidative Stress, Neuroprotective Agents, Infarction, Middle Cerebral Artery, MAP Kinase Signaling System, Rats, Membrane Potential, Mitochondrial
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