ArticlePharmacological reports : PR2020
Hexahydrocurcumin alleviated blood-brain barrier dysfunction in cerebral ischemia/reperfusion rats.
Article in Pharmacological reports : PR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 33 citations in OpenAlex.
- Toxicity evaluation and anti-ischemic stroke activity of selected natural extracts in zebrafish.Biomedical reports · 2026Article
- Artificial intelligence and machine learning for precision prevention of cognitive decline: integrating multimodal biomarkers, lifestyle interventions, and natural medicines from prediction to clinical practice.Frontiers in aging neuroscience · 2026Review
- Neuroprotective potential of indian herbs in ischaemic stroke: a comprehensive review of pharmacological insights, therapeutic gaps, and future directions.Inflammopharmacology · 2025Review
- Galangin's Neuroprotective Role: Targeting Oxidative Stress, Inflammation, and Apoptosis in Ischemic Stroke in a Rat Model of Permanent Middle Cerebral Artery Occlusion.International journal of molecular sciences · 2025Article
- Article
- Hexahydrocurcumin Attenuates Neuronal Injury and Modulates Synaptic Plasticity in Chronic Cerebral Hypoperfusion in Rats.Molecular neurobiology · 2024Article
- Hexahydrocurcumin attenuated demyelination and improved cognitive impairment in chronic cerebral hypoperfusion rats.Inflammopharmacology · 2024Article
- Article
- Research progress on the mechanism of curcumin in cerebral ischemia/reperfusion injury: a narrative review.Apoptosis : an international journal on programmed cell death · 2023Review
- Melatonin suppresses inflammation and blood‒brain barrier disruption in rats with vascular dementia possibly by activating the SIRT1/PGC-1α/PPARγ signaling pathway.Inflammopharmacology · 2023Article
- Luteolin alleviates inflammation and autophagy of hippocampus induced by cerebral ischemia/reperfusion by activating PPAR gamma in rats.BMC complementary medicine and therapies · 2022Article
- Mechanisms Underlying Curcumin-Induced Neuroprotection in Cerebral Ischemia.Frontiers in pharmacology · 2022Review
- Curcumin Efficacy in a Serum/Glucose Deprivation-Induced Neuronal PC12 Injury Model.Current molecular pharmacology · 2021Article
- Histo-ELISA technique for quantification and localization of tissue components.Scientific reports · 2020Article
- Transplanted hair follicle stem cells migrate to the penumbra and express neural markers in a rat model of cerebral ischaemia/reperfusion.Stem cell research & therapy · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHexahydrocurcumin (HHC), a major metabolite of curcumin, has been reported to have protective effects against ischemic and reperfusion damage. The goal of the present research was to examine whether HHC could alleviate brain damage and ameliorate functional outcomes by diminishing the blood-brain barrier (BBB) damage that follows cerebral ischemia/reperfusion.
methodsMiddle cerebral artery occlusion was induced for 2 h in rats followed by reperfusion. The rats were divided into three groups: sham-operated, vehicle-treated, and HHC-treated groups. At the onset of reperfusion, the rats were immediately intraperitoneally injected with 40 mg/kg HHC. At 48 h after reperfusion, the rats were evaluated for neurological deficits and TTC staining. At 24 h and 48 h after reperfusion, animals were sacrificed, and their brains were extracted.
resultsTreatment with HHC reduced neurological scores, infarct volume, morphological changes, Evans blue leakage and immunoglobulin G extravasation. Moreover, HHC treatment reduced BBB damage and neutrophil infiltration, downregulated myeloperoxidase, ICAM-1, and VCAM-1, upregulated tight junction proteins (TJPs), and reduced aquaporin 4 expression and brain water content.
conclusionThese results revealed that HHC treatment preserved the BBB from cerebral ischemia/reperfusion injury by regulating TJPs, attenuating neutrophil infiltration, and reducing brain edema formation.
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