ArticleFrontiers in neuroscience2016
Sinomenine Provides Neuroprotection in Model of Traumatic Brain Injury via the Nrf2-ARE Pathway.
Article in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Artificial Intelligence-Based Approaches for Brain Tumor Segmentation in MRI: A Review.NMR in biomedicine · 2025Review
- Sinomenine Modifies Parkinson's Disease Through Nrf2 Activation.Neurochemical research · 2025Article
- Sinomenine Inhibits TOPK To Ameliorate Psoriasiform Dermatitis.ACS omega · 2025Article
- Protective effect of sinomenine against CCl4-induced acute liver injury through regulation of mitochondrial biogenesis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Ferroptosis in Cognitive Impairment Associated with Diabetes and Alzheimer's Disease: Mechanistic Insights and New Therapeutic Opportunities.Molecular neurobiology · 2025Review
- Severity of Repetitive Mild Traumatic Brain Injury Depends on Microglial Heme Oxygenase-1 and Carbon Monoxide.The European journal of neuroscience · 2025Article
- Bioactivities and Mechanisms of Action of Sinomenine and Its Derivatives: A Comprehensive Review.Molecules (Basel, Switzerland) · 2024Review
- Research Progress on Neuroprotective Effects of Isoquinoline Alkaloids.Molecules (Basel, Switzerland) · 2023Review
- Review
- Potential therapeutic effects and pharmacological evidence of sinomenine in central nervous system disorders.Frontiers in pharmacology · 2022Review
- Targeting Nrf2-Mediated Oxidative Stress Response in Traumatic Brain Injury: Therapeutic Perspectives of Phytochemicals.Oxidative medicine and cellular longevity · 2022Review
- Promise of the NLRP3 Inflammasome Inhibitors in In Vivo Disease Models.Molecules (Basel, Switzerland) · 2021Review
- Cellular Mechanisms Participating in Brain Repair of Adult Zebrafish and Mammals after Injury.Cells · 2021Review
- Novel Synthetic and Natural Therapies for Traumatic Brain Injury.Current neuropharmacology · 2021Review
- Xiaochaihutang Improves the Cortical Astrocyte Edema in Thioacetamide-Induced Rat Acute Hepatic Encephalopathy by Activating NRF2 Pathway.Frontiers in pharmacology · 2020Article
- Sinomenine Attenuates Traumatic Spinal Cord Injury by Suppressing Oxidative Stress and Inflammation via Nrf2 Pathway.Neurochemical research · 2019Article
- Rosmarinic acid elicits neuroprotection in ischemic strokeNeural regeneration research · 2018Article
- Ischemic Postconditioning Alleviates Cerebral Ischemia-Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats.Neurochemical research · 2018Article
- Docosahexaenoic Acid (DHA) Provides Neuroprotection in Traumatic Brain Injury Models via Activating Nrf2-ARE Signaling.Inflammation · 2018Article
- Protective Effects of Sinomenine Against Ankylosing Spondylitis and the Underlying Molecular Mechanisms.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuroprotective effect of sinomenine (SIN) has been demonstrated in several brain injury models. However, its role and molecular mechanism in traumatic brain injury (TBI) remain unknown. In this study, we investigated the neuroprotective effects of SIN in the weight-drop model of TBI in male ICR mice. Mice were randomly divided into the sham and TBI groups, SIN (10 mg/kg, 30 mg/kg and 50 mg/kg, administered intraperitoneally) or equal volume of vehicle was given at 30 min after TBI. Treatment with 30 mg/kg SIN significantly improved motor performance and alleviated cerebral edema. However, treatment with 10 mg/kg or 50 mg/kg SIN did not exhibit a better outcome. Therefore, we chose 30 mg/kg SIN for our subsequent experiments. SIN significantly increased the expression of Bcl-2 and decreased that of cleaved caspase-3, indicating that SIN is anti-apoptotic. This was confirmed by the observation that SIN-treated animals had fewer apoptotic neurons. Cortical malondialdehyde content, glutathione peroxidase (GPx) activity and superoxide dismutase (SOD) activity were restored in the group that received SIN. Furthermore, Western blot and immunofluorescence experiments showed that SIN enhanced the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to the nucleus. SIN administration also significantly upregulated the expression of the downstream factors heme oxygenase 1 and NAD(P)H:quinone oxidoreductase 1 at pre- and post-transcriptional levels. Together, these data demonstrate that SIN exerts a neuroprotective effect in a model of TBI, possibly by activating the Nrf2-antioxidant response element (ARE) pathway.
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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 OpenQuestion graph.