Protective Effect of Taurine against Reperfusion Injury in Cultured Rat Astrocytes

1996 ◽  
pp. 491-497 ◽  
Author(s):  
Toshio Matsuda ◽  
Kazuhiro Takuma ◽  
Yoko Kishida ◽  
Junichi Azuma ◽  
Akemichi Baba
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Rat Astrocytes

Protective effect of dl-3n-butylphthalide preconditioning on focal cerebral ischaemia-reperfusion injury in rats

2013 ◽  
Vol 25 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Pei-Lei Zhang ◽  
Hai-Tao Lu ◽  
Jun-Gong Zhao ◽  
Ming-Hua Li
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Neurological Deficit ◽  
Cerebral Ischaemia ◽  
Sham Operation ◽  
Focal Cerebral Ischaemia ◽  
Vegf Expression ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Infarction Volume

ObjectiveTo investigate the effect of dl-3n-butylphthalide (NBP) on the protection of cerebral tissue and possible mechanism on ischaemia-reperfusion injury, and to find out whether NBP therapy can extend the reperfusion window in an experimental stroke model in rats.MethodsSeventy-two Sprague-Dawley rats were randomly divided into sham operation, ischaemia-reperfusion and ischaemia-reperfusion with NBP groups. Focal cerebral ischaemia was induced using the modified intraluminal thread method and maintained for 2, 3 or 4 h. The ischaemia-reperfusion group received reperfusion immediately after ischaemia-reperfusion. The NBP group received intraperitoneal injection of NBP immediately after ischaemia, followed by reperfusion. The sham operation group received only injection of physiological saline. The cerebral infarction volume and neurological deficit were analysed, and vascular endothelial growth factor (VEGF) expression in brain tissues was visualised by immunohistochemistry.ResultsNBP treatment caused a significant decrease in both infarction volume and neurological deficit compared with the ischaemia-reperfusion group at corresponding time points in each (p < 0.05). In the NBP group, the infarction volume and neurological deficit did not change with different ischaemia times. The expression of VEGF was significantly decreased in the ischaemia-reperfusion group compared with the sham group (p < 0.01), while this change was partly prevented in the NBP group (p < 0.01). The expression of VEGF in brain tissue in both the NBP and ischaemia-reperfusion groups gradually decreased when the ischaemic period was prolonged.ConclusionNBP treatment has a protective effect against cerebral ischaemia; this possible mechanism maybe related to the VEGF expression and may extend the reperfusion window for subsequent salvage of cerebral ischaemia by reperfusion.

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