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Lyoniresinol Attenuates Cobalt-Induced Neurobehavioral Deficits and Inflammatory Responses Associated With
Yuming Zhang1, Jun Wang2, Qifan Huo1
1Department of Anesthesiology, Shaanxi Provincial People's Hospital, Xi'an, China.
Journal of Biochemical and Molecular Toxicology
|May 14, 2026
Summary
Lyoniresinol offers neuroprotection against cobalt toxicity by improving memory, reducing inflammation, and restoring brain chemistry. This natural lignan mitigates cobalt-induced neurodegeneration through antioxidant and anti-inflammatory pathways.
Area of Science:
- Neuroscience
- Toxicology
- Pharmacology
Background:
- Cobalt exposure is an emerging neurotoxic threat with unclear mechanisms and treatments.
- Neurodegeneration induced by cobalt poses significant health risks in industrial and medical settings.
- Natural compounds with antioxidant and anti-inflammatory properties are being explored for neuroprotection.
Purpose of the Study:
- To investigate the neuroprotective potential of Lyoniresinol against cobalt-induced neurodegeneration in a rat model.
- To elucidate the underlying mechanisms of Lyoniresinol's effects on oxidative stress, inflammation, and neurotransmitter balance.
- To evaluate the impact of Lyoniresinol on cognitive function, anxiety, and motor coordination in cobalt-exposed rats.
Main Methods:
- Rats were exposed to cobalt chloride (CoCl₂) and co-treated with Lyoniresinol.
- Behavioral tests included Morris water maze, novel object recognition, elevated plus maze, and rotarod test.
- Biochemical assays measured antioxidant enzymes (SOD, GSH, MDA), inflammatory cytokines (IL-1β, IL-6, TNF-α, CRP), neurotransmitters (dopamine, serotonin, GABA), and molecular pathways (NF-κB, GSK3β, JNK) via qPCR and Western blot.
Main Results:
- Lyoniresinol significantly improved spatial and recognition memory, reduced anxiety, and enhanced motor coordination.
- Biochemical analysis showed enhanced antioxidant defense, suppressed inflammation, and normalized neurotransmitter levels.
- Histopathology confirmed neuronal preservation, and molecular analysis revealed downregulation of NF-κB, GSK3β, and JNK signaling pathways.
Conclusions:
- Lyoniresinol demonstrates significant neuroprotective effects against cobalt-induced neurotoxicity.
- The compound ameliorates behavioral deficits by reducing oxidative stress, inflammation, and neurotransmitter imbalances.
- Lyoniresinol's mechanism involves the modulation of key intracellular signaling pathways, offering a promising therapeutic strategy.
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