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Updated: Feb 15, 2026

Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice
Published on: August 22, 2011
Sinomenine reduces neuronal cell apoptosis in mice after traumatic brain injury via its effect on mitochondrial
Chuanjing Fu1, Qi Wang2, Xiaofu Zhai3
1Department of Neurosurgery, Jiangsu Hospital of Traditional Chinese Medicine, Nanjing.
Background:
Sinomenine (SIN) has been shown to have protective effects against brain damage following traumatic brain injury (TBI). However, the mechanisms and its role in these effects remain unclear. This study was conducted to investigate the potential mechanisms of the protective effects of SIN.
Methods:
The weight-drop model of TBI in Institute of Cancer Research (ICR) mice were treated with SIN or a vehicle via intraperitoneal administration 30 min after TBI. All mice were euthanized 24 h after TBI and after neurological scoring, a series of tests were performed, including brain water content and neuronal cell death in the cerebral cortex.
Results:
The level of cytochrome c (Cyt c), malondialdehyde (MDA), glutathione peroxidase (GPx) and superoxide dismutase 1 (SOD) were restored to some degree following the SIN treatment. The SIN treatment significantly decreased caspase-3 expression and reduced the number of positive cells by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay and improved the survival of neuronal cells. Additionally, the pretreatment levels of MDA were restored, while Bax translocation to mitochondria and Cyt c release into the cytosol were reduced by the SIN treatment.
Conclusion:
SIN protected neuronal cells by protecting them against apoptosis via mechanisms that involve the mitochondria following TBI.
Insights
Sinomenine (SIN) protects brain cells after traumatic brain injury (TBI) by reducing cell death. This study investigated SIN's mechanisms, finding it inhibits apoptosis and protects neurons.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Traumatic brain injury (TBI) can cause significant brain damage.
- Sinomenine (SIN) shows potential neuroprotective effects, but its mechanisms are not fully understood.
Purpose of the Study:
- To investigate the underlying mechanisms of SIN's neuroprotective effects in a TBI model.
- To elucidate SIN's role in mitigating neuronal damage and apoptosis post-TBI.
Main Methods:
- A weight-drop TBI model was established in ICR mice.
- Mice received intraperitoneal SIN or vehicle 30 minutes post-TBI.
- Evaluated neurological scores, brain water content, neuronal cell death (TUNEL assay), and specific protein expressions (cytochrome c, caspase-3, Bax, MDA, GPx, SOD).
Main Results:
- SIN treatment partially restored levels of cytochrome c, MDA, GPx, and SOD.
- SIN significantly reduced caspase-3 expression and TUNEL-positive cells, indicating decreased apoptosis.
- SIN treatment inhibited Bax translocation to mitochondria and cytochrome c release, improving neuronal survival.
Conclusions:
- SIN demonstrates neuroprotective effects against TBI by inhibiting mitochondrial-mediated apoptosis.
- The findings suggest SIN is a promising therapeutic agent for TBI treatment.
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