ArticleCell death & disease2013
Anthraquinone-2-sulfonic acid (AQ2S) is a novel neurotherapeutic agent.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 61 citations in OpenAlex.
- Sulfone-quinone derivatives: a review on their synthetic methods, properties and applications.RSC advances · 2026Review
- Effect of Substituents on Solubility, Medicinal, Absorption, Emission and Cationic/Anionic Detection Properties of Anthraquinone Derivatives.Journal of fluorescence · 2024Review
- Virtual Screening of a Library of Naturally Occurring Anthraquinones for Potential Anti-Fouling Agents.Molecules (Basel, Switzerland) · 2023Article
- PHLPP Inhibitor NSC74429 Is Neuroprotective in Rodent Models of Cardiac Arrest and Traumatic Brain Injury.Biomolecules · 2022Article
- Adjusting the Structure of β-Cyclodextrin to Improve Complexation of Anthraquinone-Derived Drugs.Molecules (Basel, Switzerland) · 2021Article
- Journey of anthraquinones as anticancer agents - a systematic review of recent literature.RSC advances · 2021Review
- Marine Anthraquinones: Pharmacological and Toxicological Issues.Marine drugs · 2021Review
- Prolongation of metallothionein induction combats Aß and α-synuclein toxicity in aged transgenic Caenorhabditis elegans.Scientific reports · 2020Article
- Kanglexin protects against cardiac fibrosis and dysfunction in mice by TGF-β1/ERK1/2 noncanonical pathway.Frontiers in pharmacology · 2020Article
- RNA Binding Motif 5 (RBM5) in the CNS-Moving Beyond Cancer to Harness RNA Splicing to Mitigate the Consequences of Brain Injury.Frontiers in molecular neuroscience · 2020Article
- Elucidation of marine fungi derived anthraquinones as mycobacterial mycolic acid synthesis inhibitors: an in silico approach.Molecular biology reports · 2019Article
- Oxidative stress induces release of 2'-AMP from microglia.Brain research · 2019Article
- Review
- Acute Physiology and Neurologic Outcomes after Brain Injury in SCOP/PHLPP1 KO Mice.Scientific reports · 2018Article
- BrainPhys® increases neurofilament levels in CNS cultures, and facilitates investigation of axonal damage after a mechanical stretch-injury in vitro.Experimental neurology · 2018Article
- Investigation of the neuroprotective effects of a novel synthetic compound via the mitochondrial pathway.Molecular medicine reports · 2017Article
- Adenosine production by brain cells.Journal of neurochemistry · 2017Article
- The nuclear splicing factor RNA binding motif 5 promotes caspase activation in human neuronal cells, and increases after traumatic brain injury in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Emerging therapies in traumatic brain injury.Seminars in neurology · 2015Review
- Evaluation of biological properties and clinical effectiveness of Aloe vera: A systematic review.Journal of traditional and complementary medicine · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Anthraquinone derivatives such as emodin have recently been shown to protect in models of beta amyloid β (Aβ) and tau aggregation-induced cell death. The mechanisms of action possibly involve preconditioning effects, anti-aggregation properties, and/or enhancing the phosphatidylinositol-3-kinase (PI3K)/AKT survival mechanism. We studied several natural (emodin, rhein, and aloin) and synthetic (AQ2S) anthraquinones, to screen for post-treatment therapeutic benefit in two models of neuronal death, namely hydrogen peroxide (H(2)O(2)) and staurosporine (STS)-induced injury. Treatment with emodin, rhein, or aloin failed to reduce H(2)O(2) injury. Moreover, consistent with emodin behaving like a mild toxin, it exacerbated oxidative injury at the highest concentration used (50 μM) in our post-treatment paradigm, and potently inhibited AKT. In contrast, AQ2S was neuroprotective. It reduced H(2)O(2) injury at 50 and 75 μM. In addition, AQ2S potently inhibited staurosporine (STS)-induced injury. The mechanisms of action involve caspase inhibition and AKT activation. However, blockade of AKT signaling with LY294002 failed to abolish AQ2S-mediated protection on the STS assay. This is the first study to report that AQ2S is a new neuroprotective compound and a novel caspase inhibitor.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.