scholarly journals Protective effects of VEGF treatment on focal cerebral ischemia in rats

2012 ◽  
Vol 6 (6) ◽  
pp. 1315-1318 ◽  
Author(s):  
AIMEI ZHANG ◽  
LUNAN LIANG ◽  
HUANFU NIU ◽  
PENG XU ◽  
YONGNAN HAO
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Protective Effects

Neuronal protective effects of focal ischemic pre- and/or postconditioning on the model of transient focal cerebral ischemia in rats

2009 ◽  
Vol 16 (5) ◽  
pp. 693-697 ◽  
Author(s):  
M. Ozgur Taskapilioglu ◽  
Tulin Alkan ◽  
Bulent Goren ◽  
Kudret Tureyen ◽  
Soner Sahin ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Protective Effects ◽  
Transient Focal Cerebral Ischemia

Dragon's blood dropping pills have protective effects on focal cerebral ischemia rats model

Phytomedicine ◽  
2013 ◽  
Vol 21 (1) ◽  
pp. 68-74 ◽  
Author(s):  
Nian Xin ◽  
Fang-Ju Yang ◽  
Yan Li ◽  
Yu-Juan Li ◽  
Rong-Ji Dai ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Protective Effects ◽  
Dragon’S Blood

Protective Effect of Astragaloside on Focal Cerebral Ischemia/Reperfusion Injury in Rats

2010 ◽  
Vol 38 (03) ◽  
pp. 517-527 ◽  
Author(s):  
Yan-Yan Yin ◽  
Wei-Ping Li ◽  
Hui-Ling Gong ◽  
Fen-Fang Zhu ◽  
Wei-Zu Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Water Content ◽  
Neurological Deficit ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Content Increase ◽  
Protective Effects ◽  
Neurological Deficit Score ◽  
Cerebral Ischemia Reperfusion

This study was to observe the neurological protective effects of astragalosides (AST) on focal cerebral ischemia-reperfusion (I/R) injury in rats and to explore its possible mechanism. Male SD rats received right middle cerebral artery occlusion for 120 min and AST (40 mg/kg) was orally administered. The rats were decapitated 1, 3, 7, and 14 days after reperfusion. The neurological deficit score, infarct volume and water content of brain were measured; the activity of superoxide dismutase (SOD), lactate dehydrogenase (LDH) and nitric oxide synthase (NOS), and the content of malondialdehyde (MDA), lactate (LD) and nitric oxide (NO) of brain tissue were detected too. The expression of inducible nitric synthase (iNOS), nerve growth factor (NGF) and tropomyosin receptor kinase A (TrkA) mRNA were measured by RT-PCR or real-time PCR. AST could significantly reduce the neurological deficit score; infract volume and water content, increase SOD and LDH activities, decrease NOS activity and MDA, LD and NO content. AST treatment could down-regulate expression of iNOS mRNA, while, NGF and TrkA mRNA were up-regulated. Our data suggest that AST have the protective effects on focal cerebral ischemia in rats at the different reperfusion time points, the mechanism may be related to the antioxidation, regulated the expressions of iNOS, NGF and TrkA mRNA.

scholarly journals PI3K/Akt Pathway Contributes to Neurovascular Unit Protection ofXiao-Xu-MingDecoction against Focal Cerebral Ischemia and Reperfusion Injury in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Rui Lan ◽  
Jun Xiang ◽  
Yong Zhang ◽  
Guo-Hua Wang ◽  
Jie Bao ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neurovascular Unit ◽  
Cerebral Infarct ◽  
Akt Pathway ◽  
Ischemia And Reperfusion ◽  
Protective Effects ◽  
Expression Levels ◽  
Infarct Area ◽  
Cerebral Ischemia And Reperfusion

In the present study, we used a focal cerebral ischemia and reperfusion rat model to investigate the protective effects ofXiao-Xu-Mingdecoction (XXMD) on neurovascular unit and to examine the role of PI3K (phosphatidylinositol 3-kinase)/Akt pathway in this protection. The cerebral ischemia was induced by 90 min of middle cerebral artery occlusion. Cerebral infarct area was measured by tetrazolium staining, and neurological function was observed at 24 h after reperfusion. DNA fragmentation assay, combined with immunofluorescence, was performed to evaluate apoptosis of neuron, astrocyte, and vascular endothelial cell which constitute neurovascular unit. The expression levels of proteins involved in PI3K/Akt pathway were detected by Western blot. The results showed that XXMD improved neurological function, decreased cerebral infarct area and neuronal damage, and attenuated cellular apoptosis in neurovascular unit, while these effects were abolished by inhibition of PI3K/Akt with LY294002. We also found that XXMD upregulated p-PDKl, p-Akt, and p-GSK3βexpression levels, which were partly reversed by LY294002. In addition, the increases of p-PTEN and p-c-Raf expression levels on which LY294002 had no effect were also observed in response to XXMD treatment. The data indicated the protective effects of XXMD on neurovascular unit partly through the activation of PI3K/Akt pathway.

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