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Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury.

Zhao B, Gao W, Hou J, Wu Y, Xia Z - Neural Regen Res (2012)

Bottom Line: The present study established global brain ischemia using the four-vessel occlusion method.However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression significantly increased, similar to results following ischemic postconditioning.Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.

ABSTRACT
The present study established global brain ischemia using the four-vessel occlusion method. Following three rounds of reperfusion for 30 seconds, and occlusion for 10 seconds, followed by reperfusion for 48 hours, infarct area, the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced. However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression significantly increased, similar to results following ischemic postconditioning. Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.

No MeSH data available.


Related in: MedlinePlus

Correlation between p-GSK-3β activity and the number of TUNEL-positive cells.(A) Linear regression between TUNEL-positive cells and activity of p-GSK-3β (r = −0.80).(B) Linear regression between cerebral infract size and activity of p-GSK-3β (r = −0.77).I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning; p-GSK-3β: phosphorylated glycogen synthase kinase-3β.
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Figure 4: Correlation between p-GSK-3β activity and the number of TUNEL-positive cells.(A) Linear regression between TUNEL-positive cells and activity of p-GSK-3β (r = −0.80).(B) Linear regression between cerebral infract size and activity of p-GSK-3β (r = −0.77).I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning; p-GSK-3β: phosphorylated glycogen synthase kinase-3β.

Mentions: As shown in Figure 4, the activity of p-GSK-3β negatively correlated with the number of TUNEL-positive cells (r = −0.80) and infarct area (r = −0.77). These data indicate that the increased phosphorylation of p-GSK-3β is attributable to the neuroprotection of IPost in the cerebral cortex.


Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury.

Zhao B, Gao W, Hou J, Wu Y, Xia Z - Neural Regen Res (2012)

Correlation between p-GSK-3β activity and the number of TUNEL-positive cells.(A) Linear regression between TUNEL-positive cells and activity of p-GSK-3β (r = −0.80).(B) Linear regression between cerebral infract size and activity of p-GSK-3β (r = −0.77).I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning; p-GSK-3β: phosphorylated glycogen synthase kinase-3β.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4308783&req=5

Figure 4: Correlation between p-GSK-3β activity and the number of TUNEL-positive cells.(A) Linear regression between TUNEL-positive cells and activity of p-GSK-3β (r = −0.80).(B) Linear regression between cerebral infract size and activity of p-GSK-3β (r = −0.77).I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning; p-GSK-3β: phosphorylated glycogen synthase kinase-3β.
Mentions: As shown in Figure 4, the activity of p-GSK-3β negatively correlated with the number of TUNEL-positive cells (r = −0.80) and infarct area (r = −0.77). These data indicate that the increased phosphorylation of p-GSK-3β is attributable to the neuroprotection of IPost in the cerebral cortex.

Bottom Line: The present study established global brain ischemia using the four-vessel occlusion method.However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression significantly increased, similar to results following ischemic postconditioning.Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.

ABSTRACT
The present study established global brain ischemia using the four-vessel occlusion method. Following three rounds of reperfusion for 30 seconds, and occlusion for 10 seconds, followed by reperfusion for 48 hours, infarct area, the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced. However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression significantly increased, similar to results following ischemic postconditioning. Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.

No MeSH data available.


Related in: MedlinePlus