ArticleBritish journal of pharmacology2017
Celastrol prevents cadmium-induced neuronal cell death by blocking reactive oxygen species-mediated mammalian target of rapamycin pathway.
Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Dexmedetomidine attenuates Alzheimer's pathogenesis by targeting the ROS-mediated XIAP-MDM2-p53 signaling axis.Frontiers in pharmacology · 2026Article
- Mitochondrial Hydrogen Peroxide Activates PTEN and Inactivates Akt Leading to Autophagy Inhibition-Dependent Cell Death in Neuronal Models of Parkinson's Disease.Molecular neurobiology · 2023Article
- Suppressed expression of ErbB3-binding protein 1 (EBP1) genes compromised the hypersensitive response cell death inPlant biotechnology (Tokyo, Japan) · 2023Article
- Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data.Journal of applied toxicology : JAT · 2023Review
- Neuroprotective Effects of Celastrol in Neurodegenerative Diseases-Unscramble Its Major Mechanisms of Action and Targets.Aging and disease · 2022Review
- Regulation of mitochondrial dysfunction induced cell apoptosis is a potential therapeutic strategy for herbal medicine to treat neurodegenerative diseases.Frontiers in pharmacology · 2022Review
- Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021Review
- The Therapeutic Potential of Celastrol in Central Nervous System Disorders: Highlights from In Vitro and In Vivo Approaches.Molecules (Basel, Switzerland) · 2021Review
- Alpha-Lipoic Acid Attenuates Cadmium- and Lead-Induced Neurotoxicity by Inhibiting Both Endoplasmic-Reticulum Stress and Activation of Fas/FasL and Mitochondrial Apoptotic Pathways in Rat Cerebral Cortex.Neurotoxicity research · 2021Article
- Mechanosensitive Piezo1 Channel Evoked-Mechanical Signals in Atherosclerosis.Journal of inflammation research · 2021Review
- Effects of myricetin against cadmium-induced neurotoxicity in PC12 cells.Toxicology research · 2021Article
- Celastrol slows the progression of early diabetic nephropathy in rats via the PI3K/AKT pathway.BMC complementary medicine and therapies · 2020Article
- Metformin attenuates cadmium-induced neuronal apoptosis in vitro via blocking ROS-dependent PP5/AMPK-JNK signaling pathway.Neuropharmacology · 2020Article
- Preincubation with a low-dose hydrogen peroxide enhances anti-oxidative stress ability of BMSCs.Journal of orthopaedic surgery and research · 2020Article
- Terpenoids as Potential Geroprotectors.Antioxidants (Basel, Switzerland) · 2020Review
- Cadmium induces mitochondrial ROS inactivation of XIAP pathway leading to apoptosis in neuronal cells.The international journal of biochemistry & cell biology · 2020Article
- Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-κB Signaling Pathway.Frontiers in neuroscience · 2020Article
- Cannabidiol Protects Dopaminergic Neuronal Cells from Cadmium.International journal of environmental research and public health · 2019Article
- Maduramicin induces cardiac muscle cell death by the ROS-dependent PTEN/Akt-Erk1/2 signaling pathway.Journal of cellular physiology · 2019Article
- Comparative analysis of in vitro neurotoxicity of methylmercury, mercury, cadmium, and hydrogen peroxide on SH-SY5Y cells.The Journal of veterinary medical science · 2019Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
background and purposeIncreasing evidence has suggested cadmium (Cd), as an inducer of ROS, is a potential pathogenic factor in human neurodegenerative diseases. Thus, it is important to find effective interventions for Cd-induced oxidative stress in the CNS. Here, we have studied the effects of celastrol, a plant-derived triterpene, on ROS production and cell death in neuronal cells, induced by Cd. EXPERIMENTAL APPROACH: PC12, SH-SY5Y cells and primary murine neurons were used to study celastrol neuroprotection against Cd-poisoning. Cd-induced changes in cell viability, apoptosis, ROS and AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway in the cells were analysed by Trypan blue exclusion, DAPI and TUNEL staining, ROS imaging, immunofluorescence staining and Western blotting. Pharmacological and genetic approaches were employed to investigate the mechanisms underlying Cd neurotoxicity.
resultsCelastrol attenuated Cd-induced apoptosis by suppressing Cd activation of mTOR, which was attributed to preventing Cd inactivation of AMPK. Inhibition of AMPK with compound C or expression of dominant negative AMPKα prevented celastrol from hindering Cd-induced dephosphorylation of AMPKα, activation of mTOR and apoptosis. Inhibition of mTOR with rapamycin or knockdown of mTOR potentiated prevention by celastrol, of Cd-induced phosphorylation of p70 S6 kinase 1/eukaryotic initiation factor 4E binding protein 1 and apoptosis. Celastrol attenuated Cd-induced cell death by suppressing induction of mitochondrial ROS. CONCLUSIONS AND IMPLICATIONS: Celastrol prevented the inactivation of AMPK by mitochondrial ROS, thus attenuating Cd-induced mTOR activation and neuronal apoptosis. Celastrol may be a promising agent for prevention of Cd-induced oxidative stress and neurodegenerative diseases.
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Registered trials
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