ReviewInflammopharmacology2025
Baicalein-mediated regulation of Nrf2/ARE, NFĸB, and MAPK signaling in Huntington's disease: a promising strategy against neuroinflammation and neurodegeneration.
Review in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Elucidation of Baicalein's Anti-Intervertebral Disc Degeneration Mechanism Through Network Pharmacology and Experimental Validation.Cell biochemistry and biophysics · 2026Article
- Nrf2 Activators in Parkinson's Disease: Modulating Mitophagy and Regulating Cuproptosis.Molecular neurobiology · 2026Review
- Study on the Mechanism of Action of Baicalein in Inhibiting the Invasion ofAntioxidants (Basel, Switzerland) · 2026Article
- Protective effect of baicalein fromFrontiers in aging neuroscience · 2026Article
- The 4E-BPs as Translational Regulators in Neurological Disorders: Molecular Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Modulation of Nrf2 and Mitochondrial Function: Pharmacological Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a progressive neurodegenerative disorder characterized by abnormal repeat of CAG expansion in the huntingtin gene, leading to mutant huntingtin protein aggregation, oxidative stress, neuroinflammation, mitochondrial dysfunction, and neuronal loss. Despite advances in understanding HD pathogenesis, effective disease-modifying treatments remain elusive. Baicalein, a bioactive flavonoid derived from Scutellaria baicalensis, has shown promising neuroprotective effects in various neurological disorders. This review explores the therapeutic potential of Baicalein in HD, focusing on its ability to modulate key pathological pathways, including oxidative stress through Nrf2 activation, neuroinflammation via NFĸB and MAPK inhibition, mitochondrial protection, apoptosis regulation, autophagy enhancement, and excitotoxicity attenuation. Preclinical evidence from in vitro and in vivo studies highlights Baicalein's ability in mitigating HD-associated neuronal damage. However, challenges related to its bioavailability and clinical translation remain. Furthermore, research is required to find out its therapeutic application and evaluate its efficacy in clinical settings. Understanding Baicalein's molecular mechanisms may offer novel insights into developing targeted therapies for HD.
Indexed as
Identifiers
40616756What Socratic holds
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 Socratic graph.