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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

IPost reduced cell death following global brain ischemia.Number of TUNEL-positive cells following global brain ischemia treated with IPost. Each bar indicates the mean ± SD of quadruplicate experiments. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test. aP < 0.01, vs. I/R group; bP < 0.01, vs. sham-surgery group.I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning
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Figure 1: IPost reduced cell death following global brain ischemia.Number of TUNEL-positive cells following global brain ischemia treated with IPost. Each bar indicates the mean ± SD of quadruplicate experiments. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test. aP < 0.01, vs. I/R group; bP < 0.01, vs. sham-surgery group.I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning

Mentions: Following TUNEL, a large number of TUNEL-positive cells were observed in the cortex of rats subjected to ischemia/reperfusion injury, whereas TUNEL-positive cells were not detected in the cortex of sham-surgery group rats. The number of TUNEL-positive cells was significantly reduced in the cortex of the IPost and ischemic preconditioning groups compared with the ischemia/reperfusion group (P < 0.01; Figure 1, supplementary Figure 1 online).


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)

IPost reduced cell death following global brain ischemia.Number of TUNEL-positive cells following global brain ischemia treated with IPost. Each bar indicates the mean ± SD of quadruplicate experiments. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test. aP < 0.01, vs. I/R group; bP < 0.01, vs. sham-surgery group.I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: IPost reduced cell death following global brain ischemia.Number of TUNEL-positive cells following global brain ischemia treated with IPost. Each bar indicates the mean ± SD of quadruplicate experiments. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test. aP < 0.01, vs. I/R group; bP < 0.01, vs. sham-surgery group.I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning
Mentions: Following TUNEL, a large number of TUNEL-positive cells were observed in the cortex of rats subjected to ischemia/reperfusion injury, whereas TUNEL-positive cells were not detected in the cortex of sham-surgery group rats. The number of TUNEL-positive cells was significantly reduced in the cortex of the IPost and ischemic preconditioning groups compared with the ischemia/reperfusion group (P < 0.01; Figure 1, supplementary Figure 1 online).

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