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Published on: July 25, 2011
Neuroprotective effect of agmatine in rats with transient cerebral ischemia using MR imaging and histopathologic
Y C Huang1, W S Tzeng, C C Wang
1Department of Radiology, Chi Mei Medical Center, Liouying, Tainan, Taiwan.
Purpose:
This study aimed to further investigate the effects of agmatine on brain edema in the rats with middle cerebral artery occlusion (MCAO) injury using magnetic resonance imaging (MRI) monitoring and biochemical and histopathologic evaluation.
Materials And Methods:
Following surgical induction of MCAO for 90min, agmatine was injected 5min after beginning of reperfusion and again once daily for the next 3 post-operative days. The events during ischemia and reperfusion were investigated by T2-weighted images (T2WI), serial diffusion-weighted images (DWI), calculated apparent diffusion coefficient (ADC) maps and contrast-enhanced T1-weighted images (CE-T1WI) during 3h-72h in a 1.5T Siemens MAGNETON Avanto Scanner. Lesion volumes were analyzed in a blinded and randomized manner. Triphenyltetrazolium chloride (TTC), Nissl, and Evans Blue stainings were performed at the corresponding sections.
Results:
Increased lesion volumes derived from T2WI, DWI, ADC, CE-T1WI, and TTC all were noted at 3h and peaked at 24h-48h after MCAO injury. TTC-derived infarct volumes were not significantly different from the T2WI, DWI-, and CE-T1WI-derived lesion volumes at the last imaging time (72h) point except for significantly smaller ADC lesions in the MCAO model (P<0.05). Volumetric calculation based on TTC-derived infarct also correlated significantly stronger to volumetric calculation based on last imaging time point derived on T2WI, DWI or CE-T1WI than ADC (P<0.05). At the last imaging time point, a significant increase in Evans Blue extravasation and a significant decrease in Nissl-positive cells numbers were noted in the vehicle-treated MCAO injured animals. The lesion volumes derived from T2WI, DWI, CE-T1WI, and Evans blue extravasation as well as the reduced numbers of Nissl-positive cells were all significantly attenuated in the agmatine-treated rats compared with the control ischemia rats (P<0.05).
Conclusion:
Our results suggest that agmatine has neuroprotective effects against brain edema on a reperfusion model after transient cerebral ischemia.
Insights
Agmatine treatment significantly reduced brain edema and neuroprotection after middle cerebral artery occlusion (MCAO) injury in rats. This study demonstrates agmatine
Area of Science:
- Neuroscience
- Biochemistry
- Radiology
Background:
- Middle cerebral artery occlusion (MCAO) is a common cause of ischemic stroke leading to brain edema.
- Investigating neuroprotective agents is crucial for mitigating stroke-induced brain damage.
Purpose of the Study:
- To evaluate the neuroprotective effects of agmatine on brain edema following MCAO injury in a rat model.
- To utilize magnetic resonance imaging (MRI) and histopathological methods for comprehensive assessment.
Main Methods:
- Rats underwent MCAO surgery, followed by agmatine administration during reperfusion and post-operative days.
- MRI techniques including T2WI, DWI, ADC maps, and CE-T1WI were employed for lesion monitoring from 3h to 72h.
- Biochemical and histopathological analyses (TTC, Nissl, Evans Blue staining) were performed for validation.
Main Results:
- Lesion volumes, assessed by MRI and TTC staining, increased post-MCAO and peaked at 24-48h.
- Agmatine treatment significantly attenuated lesion volumes, reduced Evans Blue extravasation, and preserved Nissl-positive cells compared to controls.
- MRI-derived lesion volumes correlated well with TTC infarct volumes, with ADC showing some discrepancies.
Conclusions:
- Agmatine exhibits significant neuroprotective effects against brain edema in a rat model of transient cerebral ischemia and reperfusion.
- These findings support agmatine as a potential therapeutic agent for stroke recovery.

