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Anisodamine Ameliorates Traumatic Brain Injury-Induced Neuroinflammation and Neurological Injury in the Animal Model
Moyun Li1, Dezhi Huang2, Wenjia Ma2
1Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Journal of Biochemical and Molecular Toxicology
|January 5, 2026
Summary
This study reveals anisodamine (ANI) as a potential treatment for traumatic brain injury (TBI). ANI demonstrated neuroprotective effects by reducing inflammation and apoptosis in TBI models, partly through modulating HMOX1. Further research is needed on its clinical application.
Area of Science:
- Neuroscience
- Bioinformatics
- Pharmacology
Background:
- Traumatic brain injury (TBI) is a significant cause of mortality and long-term disability.
- Understanding the molecular mechanisms underlying TBI is crucial for developing effective treatments.
- Anisodamine (ANI) is being investigated for its potential therapeutic properties.
Purpose of the Study:
- To elucidate the molecular mechanisms of TBI using bioinformatics approaches.
- To explore the neuroprotective effects of anisodamine (ANI) in TBI.
- To identify key molecular targets and pathways involved in TBI pathogenesis and ANI's action.
Main Methods:
- Bioinformatic analysis of TBI-related microarray datasets (GSE59645, GSE111452, GSE58484) to identify differentially expressed genes (DEGs).
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses.
- Construction of protein-protein interaction (PPI) and pharmacological networks using Cytoscape.
- Molecular docking, molecular dynamics simulations, and cellular thermal shift assays to validate drug-target interactions (ANI and HMOX1).
- In vitro studies using LPS-induced microglia activation and in vivo studies using controlled cortical impact (CCI) TBI mouse models.
Main Results:
- Identified 248 TBI-related DEGs, significantly associated with inflammatory responses.
- Identified 6 core genes (CCL2, CD44, TIMP1, SERPINE1, HMOX1, CCNA2) and confirmed binding activity of ANI with these targets.
- In vitro: ANI inhibited microglia activation, reduced neuroinflammation and apoptosis, partly via HMOX1 modulation.
- In vivo: ANI treatment significantly improved neurological function and reduced neuronal apoptosis in TBI mice.
Conclusions:
- Anisodamine (ANI) exhibits significant neuroprotective effects against secondary injury in TBI.
- ANI's mechanism involves the modulation of inflammatory responses and apoptosis, with HMOX1 identified as a key target.
- ANI presents a promising therapeutic option for TBI, warranting further investigation into its clinical application, including treatment windows and safety profiles.
