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Updated: Jun 10, 2026

A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats
Published on: November 6, 2019
Neuroprotection by S-PBN in hyperglycemic ischemic brain injury in rats
Maria Molnar1, Fredrik Lennmyr
1Department of Surgical Sciences, Section of Anesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, Sweden. maria.molnar@akademiska.se
Background:
Hyperglycemia exacerbates focal ischemic brain damage supposedly through various mechanisms. One such mechanism is oxidative stress involving reactive oxygen and nitrogen species (RONS) production. Nitrones attenuate oxidative stress in various models of brain injury. Sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) can be administered experimentally and has been shown to be neuroprotective in experimental brain trauma.
Aims Of The Study:
We hypothesized that S-PBN might be neuroprotective in hyperglycemic focal cerebral ischemia.
Material And Methods:
Rats were made hyperglycemic by an intraperitoneal bolus injection of glucose (2 g/kg) and then subjected to 90 min transient middle cerebral artery occlusion (MCAO). They were randomized to a therapeutic regime of S-PBN (156 mg/kg) or saline given intravenously. Neurological testing according to Bederson and tetrazolium red staining were performed after 1 day.
Results:
S-PBN improved the neurological performance at day 1 both in Bederson score (1.3+/-0.8 versus 2.7+/-0.48) and on the inclined plane (74.5%+/-4.6 (S-PBN) versus 66%+/-8.3 (control), P<0.05) but did not reduce the infarct size. Physiological data did not differ between groups.
Conclusion:
S-PBN may improve neurological performance at short-term survival (1 day) in the present model of hyperglycemic-ischemic brain injury in rats. This effect appeared not to be primarily related to reduced infarct size.
Insights
Sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) improved neurological function in rats with hyperglycemic stroke. This neuroprotection occurred without reducing brain infarct size, suggesting a mechanism beyond tissue damage reduction.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Oxidative Stress Research
Background:
- Hyperglycemia worsens focal ischemic brain damage, potentially via oxidative stress from reactive oxygen and nitrogen species (RONS).
- Nitrones, like Sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN), are known to mitigate oxidative stress and show neuroprotective effects in brain injury models.
Purpose of the Study:
- To investigate the potential neuroprotective effects of S-PBN in a rat model of hyperglycemic focal cerebral ischemia.
Main Methods:
- Rats were induced into hyperglycemia using a glucose injection and subjected to transient middle cerebral artery occlusion (MCAO).
- Animals received intravenous S-PBN or saline treatment.
- Neurological function (Bederson score, inclined plane test) and infarct size (tetrazolium red staining) were assessed at 1 day post-occlusion.
Main Results:
- S-PBN treatment significantly improved neurological scores at day 1 compared to controls.
- Despite functional improvements, S-PBN did not significantly reduce the infarct volume.
- No significant differences in physiological parameters were observed between the S-PBN and control groups.
Conclusions:
- S-PBN demonstrates short-term neuroprotective effects in a rat model of hyperglycemic ischemic stroke.
- The observed neurological improvement is not primarily attributed to a reduction in infarct size.
- Further research is needed to elucidate the precise mechanisms underlying S-PBN's neuroprotective action in this context.
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