ArticleMediators of inflammation2014
Chrysophanol inhibits NALP3 inflammasome activation and ameliorates cerebral ischemia/reperfusion in mice.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 128 citations in OpenAlex.
- Advances and Therapeutic Potential of Anthraquinone Compounds in Neurodegenerative Diseases: A Comprehensive Review.Drug design, development and therapy · 2026Review
- The ketogenic diet alleviates autoimmune thyroiditis caused by Th17/Treg imbalance by inhibiting the HMGB1/NLRP3 signaling pathway.PloS one · 2026Article
- NLRP3 inflammasome in neuroinflammation and central nervous system diseases.Cellular & molecular immunology · 2025Review
- Inhibition of YIPF2 Improves the Vulnerability of Oligodendrocytes to Human Islet Amyloid Polypeptide.Neuroscience bulletin · 2024Article
- Article
- Hydrogen-Rich Saline-A Novel Neuroprotective Agent in a Mouse Model of Experimental Cerebral Ischemia via the ROS-NLRP3 Inflammasome Signaling Pathway In Vivo and In Vitro.Brain sciences · 2023Article
- Screening of key functional components of Taohong Siwu Decoction on ischemic stroke treatment based on multiobjective optimization approach and experimental validation.BMC complementary medicine and therapies · 2023Article
- Zishen Yutai Pill improves sperm quality and reduces testicular inflammation in experimental varicocele rats.Heliyon · 2023Article
- Bioactive Secondary Metabolites from Fungi of the GenusMolecules (Basel, Switzerland) · 2023Review
- Key insights into secondary metabolites from various Chaetomium species.Applied microbiology and biotechnology · 2023Review
- Geniposide protected against cerebral ischemic injury through the anti-inflammatory effect via the NF-κB signaling pathway.Translational neuroscience · 2023Article
- The role of NLRP3 inflammasome-mediated pyroptosis in ischemic stroke and the intervention of traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- Liraglutide Ameliorates Cerebral Ischemia in Mice via Antipyroptotic Pathways.Neurochemical research · 2022Article
- Effects of Anthraquinones on Immune Responses and Inflammatory Diseases.Molecules (Basel, Switzerland) · 2022Review
- Novel derivatives of eugenol as potent anti-inflammatory agentsRSC advances · 2022Article
- Article
- Neuroinflammation and COVID-19 Ischemic Stroke Recovery-Evolving Evidence for the Mediating Roles of the ACE2/Angiotensin-(1-7)/Mas Receptor Axis and NLRP3 Inflammasome.International journal of molecular sciences · 2022Review
- Chrysophanol Ameliorates Hemin-Induced Oxidative Stress and Endoplasmic Reticulum Stress by Regulating MicroRNA-320-5p/Wnt3a Pathway in HT22 Cells.Oxidative medicine and cellular longevity · 2022Article
- Caspase-1: A Promising Target for Preserving Blood-Brain Barrier Integrity in Acute Stroke.Frontiers in molecular neuroscience · 2022Review
- The Role of PKC and HIF-1 and the Effect of Traditional Chinese Medicinal Compounds on Cerebral Ischemia-Reperfusion Injury.Evidence-based complementary and alternative medicine : eCAM · 2022Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most effective way to contain cerebral ischemic injury is reperfusion; however, reperfusion itself may result in tissue injury, for which inflammatory damage is one of the main causative factors. NALP3 inflammasome is a multiprotein complex. It consists of NALP3, ASC, and caspase-1, whose function is to switch on the inflammatory process. Chrysophanol is an extract from plants of Rheum genus and it possesses many pharmacological effects including its anti-inflammation activity. In this study, the effects of chrysophanol in cerebral ischemia/reperfusion and the potential mechanisms were investigated. Male CD1 mice were subject to transient middle cerebral artery occlusion (tMCAO). The NALP3 inflammasome activation status and its dynamic expression during the natural inflammatory response induced by tMCAO were first profiled. The neuroprotective effects of chrysophanol were then assessed and the potential mechanisms mediating the observed neuroprotection were then explored. Physical parameters including neurological deficit, infarct size, brain edema, and BBB permeability were measured at 24 h after tMCAO. Confocal microscopy, Western blotting, immunohistochemistry, and qRT-PCR techniques were utilized to analyze the expression of NALP3 inflammasome and IL-1 β . Our results indicated that the brain tissue damage during cerebral ischemia/reperfusion is accompanied by NALP3 inflammasome activation. Chrysophanol could inhibit the activation of NALP3 inflammasome and protect cerebral ischemic stroke.
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