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The protective effect of rosuvastatin on ischemic brain injury and its mechanism
Hongyi Xing1, Shenggang Sun, Yuanwu Mei
1Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Abstract:
To study the protective effect of rosuvastatin on ischemic brain injury and its mechanism, focal cerebral ischemia/reperfusion was induced by occlusion of the middle cerebral artery (MCA) using the intra-luminal filament technique. The cerebral blood flow was monitored with laser-Doppler flowmetry (LDF). The slices of brain tissue were stained with cresyl-violet. The cerebral volume of infarction and edema were quantified with Image J software. The expressions of endothelial NO synthase (eNOS) and activated caspase-3 were detected with Western blot. The inducible NO synthase (iNOS) positive cells were immunohistochemically observed. The results demonstrated that rosuvastatin (20 mg/kg) could remarkably decrease infarct volume and cerebral edema after MCAO 90 min/reperfusion 24 h. Western blots showed that the expression of eNOS in cerebral cortex before and after ischemia was (100+/-43.3) %, (1668.9+/-112.2) % respectively (P<0.001), rosuvastatin significantly up-regulated the expression of eNOS in non-ischemic cortex (P<0.001), whereas in ischemic cortex of rosuvastatin group the expression of eNOS was (1678.8+/-121.3) %. There was no expression of activated caspase-3 in non-ischemic cortex, nonetheless the expression of activated caspase-3 increased after ischemia, and rosuvastatin significantly diminished it (P<0.01). Immunohistochemistry revealed no iNOS-positive cells in non-ischemic brain area, while in ischemic brain area the number of iNOS positive cells went up, and rosuvastatin could significantly reduced them. Consequently, the mechanisms of rosuvastatin's neural protection on ischemic brain injury are to enhance expression of eNOS, to inhibit expression of iNOS and activated caspase-3.
Insights
Rosuvastatin protects against ischemic brain injury by reducing infarct volume and cerebral edema. It achieves this by enhancing endothelial nitric oxide synthase (eNOS) and inhibiting inducible nitric oxide synthase (iNOS) and activated caspase-3.
Area of Science:
- Neuroscience
- Pharmacology
- Cardiovascular Research
Background:
- Ischemic brain injury, a major cause of stroke, results from disrupted blood flow.
- Understanding protective mechanisms is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the neuroprotective effects of rosuvastatin on ischemic brain injury.
- To elucidate the underlying molecular mechanisms involving nitric oxide synthases and apoptosis.
Main Methods:
- Focal cerebral ischemia/reperfusion induced via middle cerebral artery occlusion (MCAO) in a rodent model.
- Cerebral blood flow monitored using laser-Doppler flowmetry.
- Infarct volume and edema quantified; expressions of eNOS, iNOS, and activated caspase-3 analyzed via Western blot and immunohistochemistry.
Main Results:
- Rosuvastatin significantly reduced infarct volume and cerebral edema post-MCAO.
- Rosuvastatin upregulated eNOS expression and downregulated iNOS and activated caspase-3 expression in ischemic brain tissue.
- No iNOS or activated caspase-3 expression was observed in non-ischemic brain areas.
Conclusions:
- Rosuvastatin exhibits significant neuroprotective effects against ischemic brain injury.
- Mechanisms include enhancing eNOS expression and inhibiting iNOS and activated caspase-3.
- Rosuvastatin represents a potential therapeutic agent for stroke recovery.
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