Middle Cerebral Artery Occlusion
|
0.100 |
Biomarker
|
disease |
BEFREE |
Rats underwent 1 h of focal cerebral ischemia followed by 23 h of reperfusion were randomly divided into 6 groups (n = 36 per group): sham- operation (S), ischemia-reperfusion (IR), propofol (P group, propofol 20 mg/kg/h at the onset of reperfusion for 2 h after 60 min of occlusion), and LY294002 (PI3K non-selective antagonist) + sham (L + S, LY294002 of 1.5 mg/kg was infused 30 min before sham operation), LY294002+ ischemia-reperfusion (L + IR, LY294002 of 1.5 mg/kg was infused 30 min before middle cerebral artery occlusion), LY294002 + IR + propofol (L + P, LY294002 of 1.5 mg/kg was infused 30 min before middle cerebral artery occlusion and propofol 20 mg/kg/h at the onset of reperfusion for 2 h after 60 min of occlusion).
|
31570094 |
2019 |
Middle Cerebral Artery Occlusion
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, Western blot analysis indicated that CIG increased the expression of BDNF/p-TrkB, NRG1/ErbB4 proteins, which further elevated PI3K p110α/p-Akt/p-mTOR signaling in the corpus callosum of MCAO rats.
|
31819458 |
2019 |
Middle Cerebral Artery Occlusion
|
0.100 |
Biomarker
|
disease |
BEFREE |
The combined therapy increased expression of VEGF and BDNF to a maximum through activating PI3K and ERK1/2 pathways in the hippocampus and frontal cortex in response to transient MCAO.
|
30245466 |
2018 |
Middle Cerebral Artery Occlusion
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MiR-124 expression, ROS content, and cell apoptosis were markedly increased, whereas the levels of PI3K, p-AKT, and Bcl-2 were markedly reduced in rat VECs from MCAO group compared with that in the sham group.
|
29424909 |
2018 |
Middle Cerebral Artery Occlusion
|
0.100 |
Biomarker
|
disease |
BEFREE |
Intra-arterial human urinary kallidinogenase alleviates brain injury in rats with permanent middle cerebral artery occlusion through PI3K/AKT/FoxO1 signaling pathway.
|
29510144 |
2018 |
Middle Cerebral Artery Occlusion
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study observed the protective effect of EGCG against neuronal injury in rat models of middle cerebral artery occlusion (MCAO) and investigated the mechanism of action of PI3K/AKT/eNOS signaling pathway.
|
29770336 |
2018 |
Middle Cerebral Artery Occlusion
|
0.100 |
Biomarker
|
disease |
BEFREE |
Diffusion weighted MRI (DWI) was performed 1 h after MCAO and rats with lesion sizes within a predetermined range were randomized to either PI3K activator or vehicle treatment arms.
|
27590139 |
2017 |
Middle Cerebral Artery Occlusion
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Compared with the MCAO group, the mRNA and protein expressions of PI3K and Bcl-2, and the protein expressions of p-Akt and p-Bad were elevated, while the mRNA and protein expressions of Bax were decreased in the DADLE and DMSO groups.
|
28645007 |
2017 |
Middle Cerebral Artery Occlusion
|
0.100 |
Biomarker
|
disease |
BEFREE |
Ninety SD rats were used in order to establish the middle cerebral artery occlusion (MCAO), among which 80 rats were randomly assigned as part of the natural recovery, natural recovery+Rp-PI3K (the rats injected with PI3K/Akt inhibitor LY294002), rehabilitation training, and rehabilitation training+Rp-PI3K groups.
|
28843352 |
2017 |
Middle Cerebral Artery Occlusion
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Methyllycaconitine treatment increased cytomembrane FGFR1 expression and GFAP/BrdU-positive cells, upregulated the levels of phosphoinositide 3-kinase (PI3K) and phospho-Akt (pAkt), decreased nuclear FGFR1 expression, decreased the number of DCX-positive cells, and reduced the levels of DCX, PSA-NCAM, and Mash1 in the SVZ of MCAO mice compared with levels in vehicle-treated MCAO mice.
|
28551702 |
2017 |