Neuroprotective effects of scutellarin on rat neuronal damage induced by cerebral ischemia/reperfusion
Abstract
Aim: To investigate the neuroprotective effect and mechanisms of scutellarin, a flavonoid extracted from Erigeron breviscapus Hand Mazz, against neuronal damage following cerebral ischemia/reperfusion.
Methods: Rats were pretreated ig with scutellarin for 7 d and then subjected to cerebral schemia/reperfusion (I/R) injury induced by a middle cerebral artery occlusion (MCAO). The infarct volume and neurological deficit were determined by TTC staining and Longa's score. The permeability of the blood-brain barrier was evaluated by measurement of the Evans blue (EB) content in the brain with a spectrophotometer. The total NOx content was determined. Nitric oxide synthase (NOS) isoforms (iNOS, eNOS, nNOS) and the key angiogenic molecules, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), were detected by Western blotting.
Results: Scutellarin significantly reduced infarct volume (P<0.05 or P<0.01), ameliorated the neurological deficit and reduced the permeability of the blood-brain barrier (BBB) (P<0.05). When rats were pretreated with scutellarin (50 or 75 mg/kg), upregulation of eNOS expression and downregulation of VEGF, bFGF, and iNOS expression was observed, whereas scutellarin had no effect on nNOS expression.
Conclusion: Scutellarin has protective effects for cerebral injury through regulating the expression of NOS isoforms and angiogenic molecules.
Keywords:
Methods: Rats were pretreated ig with scutellarin for 7 d and then subjected to cerebral schemia/reperfusion (I/R) injury induced by a middle cerebral artery occlusion (MCAO). The infarct volume and neurological deficit were determined by TTC staining and Longa's score. The permeability of the blood-brain barrier was evaluated by measurement of the Evans blue (EB) content in the brain with a spectrophotometer. The total NOx content was determined. Nitric oxide synthase (NOS) isoforms (iNOS, eNOS, nNOS) and the key angiogenic molecules, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), were detected by Western blotting.
Results: Scutellarin significantly reduced infarct volume (P<0.05 or P<0.01), ameliorated the neurological deficit and reduced the permeability of the blood-brain barrier (BBB) (P<0.05). When rats were pretreated with scutellarin (50 or 75 mg/kg), upregulation of eNOS expression and downregulation of VEGF, bFGF, and iNOS expression was observed, whereas scutellarin had no effect on nNOS expression.
Conclusion: Scutellarin has protective effects for cerebral injury through regulating the expression of NOS isoforms and angiogenic molecules.