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Updated: Apr 1, 2026
A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats
Published on: November 6, 2019
Neuroprotective effects of Aceglutamide on motor function in a rat model of cerebral ischemia and reperfusion
Purpose:
To investigate the effect and underlying mechanism of Aceglutamide on motor dysfunction in rats after cerebral ischemia-reperfusion.
Methods:
Adult male Sprague-Dawley rats were subjected to 2 h transient middle cerebral artery occlusion (MCAO). Aceglutamide or vehicle was intraperitoneally given to rats at 24 h after reperfusion and lasted for 14 days. Subsequently functional recovery was assessed and number of tyrosine hydroxylase (TH)-positive neurons in substantia nigra (SN) was analyzed. Tumor necrosis factor receptor-associated factor 1(TRAF1), P-Akt and Bcl-2/Bax were determined in mesencephalic tissue by Western blot method. PC12 cells and primary cultured mesencephalic neurons were employed to further investigate the mechanism of Aceglutamide.
Results:
Aceglutamide treatment improved behavioral functions, reduced the infarction volume, and elevated the number of TH-positive neurons in the SN. Moreover, Aceglutamide significantly attenuated neuronal apoptosis in the SN. Meanwhile Aceglutamide treatment significantly inhibited the expression of TRAF1 and up-regulated the expression of P-Akt and Bcl-2/Bax ratio both in vitro and in vivo.
Conclusions:
Aceglutamide ameliorated motor dysfunction and delayed neuronal death in the SN after ischemia, which involved the inhibition of pro-apoptotic factor TRAF1 and activation of Akt/Bcl-2 signaling pathway. These data provided experimental information for applying Aceglutamide to ischemic stroke treatment.
Insights
Aceglutamide improved motor function and reduced brain damage in rats after stroke. It protected neurons by inhibiting TRAF1 and activating the Akt/Bcl-2 pathway, suggesting potential for ischemic stroke treatment.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Cerebral ischemia-reperfusion causes motor dysfunction.
- Neuronal death in the substantia nigra (SN) contributes to motor deficits.
Purpose of the Study:
- To investigate Aceglutamide's effect on motor dysfunction post-cerebral ischemia-reperfusion.
- To elucidate the underlying mechanism of Aceglutamide's neuroprotective action.
Main Methods:
- Rats underwent middle cerebral artery occlusion (MCAO) followed by Aceglutamide treatment.
- Functional recovery, TH-positive neuron counts, and protein expression (TRAF1, P-Akt, Bcl-2/Bax) were assessed.
- In vitro studies using PC12 cells and primary neurons further explored mechanisms.
Main Results:
- Aceglutamide improved behavioral functions and reduced infarction volume.
- It increased tyrosine hydroxylase (TH)-positive neurons in the SN and attenuated neuronal apoptosis.
- Aceglutamide inhibited TRAF1 and upregulated P-Akt and Bcl-2/Bax expression.
Conclusions:
- Aceglutamide ameliorates motor dysfunction and delays neuronal death in the SN after ischemia.
- The mechanism involves inhibiting TRAF1 and activating the Akt/Bcl-2 signaling pathway.
- Aceglutamide shows promise for ischemic stroke treatment.
