Abstract
This study was designed to investigate the protective effect of ferulic acid (FA) on nerve injury induced by cerebral ischemia. Focal cerebral ischemia was induced by occlusion of the right middle cerebral artery and reperfusion 90 min later in male Sprague-Dawley rats. Daily treatment of the rats with FA was initiated 30 min after the surgery, and was continued for 7 days. The efficacy of FA against nerve injury was assessed by neurological deficit scores as well as pathohistological observation. The expression levels in the brain and level in the peripheral blood of erythropoietin (EPO) and granulocyte colony-stimulating factor (G-CSF) were analyzed by immunohistochemistry and enzyme-linked immunosorbent assay (ELISA), respectively. The results showed that FA attenuated nerve injury of the hippocampus, significantly ameliorated neurological deficits, and increased EPO but not G-CSF expression in the hippocampus and the peripheral blood of ischemic rats. The findings indicate that FA has certain protective effects on the nerve injury of cerebral ischemia, and suggest that promoting EPO in the brain and peripheral blood may be one of the neuroprotective mechanisms of FA.
Highlights
Stroke is a serious threat to human health, and is recognized as the most important factor resulting in nerve injury [1,2]
The results showed that EPO expression within the infarct region in the vehicle-treated group was significantly increased compared with that of the sham‐operated group
With regard to granulocyte colony‐stimulating factor (G-CSF), cerebral ischemia induced a significant increase in its expression, whereas treatment with Ferulic acid (FA) was not observed to induce a significant difference in the expression of the protein in the infarct region compared with that in the vehicle-treated rats (Fig. 2)
Summary
Stroke is a serious threat to human health, and is recognized as the most important factor resulting in nerve injury [1,2]. Evidence suggests that nerve injury occurs following ischemia in susceptible brain regions, such as the hippocampus and the cerebral cortex. Neuronal cell death has been identified by morphological analysis of the ischemic brain, and genetic and biochemical evidence further support the association of neuronal cell death with ischemia [3,4]. The chemical constituents of the extract of the roots of Angelica sinensis are classified into essential oil‐ and water‐soluble materials [7]. Previous studies have demonstrated that FA is able to enhance hematopoietic progenitor cell activity resulting in accelerated blood cell recovery by stimulating erythropoietin (EPO) and granulocyte colony‐stimulating factor (G-CSF) expression [8,9]. A further study demonstrated that FA was able to reduce cerebral infarction in a model of transient middle cerebral artery occlusion [10]
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