Abstract
This study investigates the impacts of n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-β1 (TGF-β1) in rats with focal cerebral ischemia. The thread embolization method was used to prepare the rat model of cerebral ischemia-reperfusion (CIR). The animals were divided into a sham operation group, a model control group and NBP treatment group. The NBP group was orally administered 25 mg/kg NBP twice a day after the surgery. The immunohistochemistry and reverse transcription-polymerase chain reaction were performed to observe the protein and mRNA expressions of VEGF and TGF-β 16 hours, 1 day and 2 days after inducing CIR. The mRNA and protein expressions of VEGF and TGF-β1 in the model control group and the NBP treatment group were all increased after CIR, and those of the NBP treatment group at each post-CIR time point were higher than the model control group (p < 0.01). After CIR, the expressions of VEGF and TGF-β1 increased, suggesting that VEGF and TGF-β1 exhibited protective effects towards the ischemic brain injuries, and that NBP could upregulate the expressions of VEGF and TGF-β1 in the peri-infarcted area, thus possibly protecting the ischemic brain tissues through this mechanism.
Highlights
Ischemic cerebrovascular disease refers to a class of diseases characterized by the softening of brain tissues, caused by brain blood supply disorders, ischemia and hypoxia [1]
The vascular endothelial growth factor (VEGF) was separated and purified by Ferrara and Henzel [2] from in vitro culture of bovine pituitary follicular astrocytes in 1989, and named VEGF because of its ability to promote the mitosis of vascular endothelial cells (VECs)
Current studies show that transforming growth factor-β1 (TGF-β1) could weaken ischemia-induced cerebral blood vessel dilation, and play an important role in the angiogenic process [6,7]
Summary
Ischemic cerebrovascular disease refers to a class of diseases characterized by the softening of brain tissues, caused by brain blood supply disorders, ischemia and hypoxia [1]. Cui et al [5] thought that, through the phosphoinositide 3-kinase/Akt signaling pathway, and prior to the formation of new blood vessels, VEGF played a role in neurotrophy and Submitted: 10 June 2015 / Accepted: 01 August 2015 nerve tissue protection, and could help to prolong the survival of cells. Current studies show that TGF-β1 could weaken ischemia-induced cerebral blood vessel dilation, and play an important role in the angiogenic process [6,7]. Investigating the regulation of expression of VEGF and TGF-β1 and their roles in ischemic brain injuries might lead to new treatment modalities. Increasing the expressions of VEGF and TGF-β1 in ischemic brain tissues may become a strategy for treating ischemic cerebrovascular diseases and a theoretical foundation for future clinical treatment
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