ArticleNeurochemical research2022
Tetrandrine Ameliorates Traumatic Brain Injury by Regulating Autophagy to Reduce Ferroptosis.
Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Old and Promising Markers Related to Autophagy in Traumatic Brain Injury.International journal of molecular sciences · 2022Pooled it
- Effects of dihydroorotate dehydrogenase inhibition and vitamin E supplementation on ferroptosis-related mechanisms and post-mortem meat quality in broiler chickens.Animal bioscience · 2026Article
- The AMPK-BECN1-System Xc⁻ Pathway in Traumatic Brain Injury: Implications for Exosome-Based Therapy.Cellular and molecular neurobiology · 2026Review
- Research Progress on Regulating Autophagy in Traditional Chinese Medicine for the Treatment of Traumatic Brain Injury.ACS omega · 2025Review
- Research progress on the use of traditional Chinese medicine to treat diseases by regulating ferroptosis.Genes & diseases · 2025Review
- Mesenchymal stem cell exosomes therapy for the treatment of traumatic brain injury: mechanism, progress, challenges and prospects.Journal of translational medicine · 2025Review
- Aminophylline targets miR-128-3p/Slc7a11 axis to attenuate neuronal ferroptosis after traumatic brain injury.Cellular and molecular life sciences : CMLS · 2025Article
- Insights on exploring the therapeutic potential and structural modification of Tetrandrine.Future medicinal chemistry · 2024Review
- Tetrandrine ameliorated atherosclerosis in vitamin D3/high cholesterol diet-challenged rats via modulation of miR-34a and Wnt5a/Ror2/ABCA1/NF-kB trajectory.Scientific reports · 2024Article
- Metformin enhances endogenous neural stem cells proliferation, neuronal differentiation, and inhibits ferroptosis through activating AMPK pathway after spinal cord injury.Journal of translational medicine · 2024Article
- Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities.Frontiers in immunology · 2024Review
- Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases.Signal transduction and targeted therapy · 2023Review
- Research Progress on Neuroprotective Effects of Isoquinoline Alkaloids.Molecules (Basel, Switzerland) · 2023Review
- Ferroptosis and Its Role in Chronic Diseases.Cells · 2022Review
- The role of regulatory necrosis in traumatic brain injury.Frontiers in molecular neuroscience · 2022Review
- Mechanism of Ferroptosis and Its Relationships with Other Types of Programmed Cell Death: Insights for Potential Therapeutic Benefits in Traumatic Brain Injury.Oxidative medicine and cellular longevity · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is the leading cause of death and disability in trauma patients. However, the effects and mechanism of autophagy after TBI remain unclear. This study aimed to investigate whether tetrandrine could ameliorate TBI through autophagy to reduce ferroptosis. A mice model for TBI was implemented. Behavioral and histomorphological experiments were performed to evaluate outcomes of the mice. The ferroptosis levels was detected by Perls staining. Enzyme-linked immunosorbent assay (ELISA) was applied to detect malondialdehyde (MDA), glutathione (GSH), and glutathione peroxidase 4 (GPX4) levels in the brain tissue. Western blot test was performed to detect Beclin 1, light chain 3 (LC3) II/I, p62, GPX4, SCL7A11, and ferritin heavy chain 1 (FTH1) levels, and the expression of LC3B, Beclin 1, GPX4, and FTH1 in the brain tissue was detected by immunofluorescence (IF). The behavioral and histomorphological results demonstrated that tetrandrine improved the neurological function and cerebral edema on days 1, 3, and 7 after TBI. The ELISA results suggested that tetrandrine reduced the MDA concentration and increased GSH concentration on days 1, 3, and 7 after TBI. IF staining and Perls staining reflected that tetrandrine promoted autophagy and inhibited ferroptosis on days 1, 3, and 7 after TBI, respectively. Tetrandrine further improved the neurological function, cerebral edema, autophagy, and ferroptosis on days 1, 3, and 7 after TBI after adding the autophagy inducer rapamycin. The effect of TET in alleviating TBI increased with the increase of time and dose. Tetrandrine ameliorated TBI by regulating autophagy to reduce ferroptosis, providing a new therapeutic strategy for TBI.
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