Limits...
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 influenced the expression of apoptosis-related proteins.Immunostaining for Bcl-2, Bax, and caspase-3. Each bar represents the mean ± SD of quadruplicate studies. aP < 0.01, vs. I/R group. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test.I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4308783&req=5

Figure 5: IPost influenced the expression of apoptosis-related proteins.Immunostaining for Bcl-2, Bax, and caspase-3. Each bar represents the mean ± SD of quadruplicate studies. aP < 0.01, vs. I/R group. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test.I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning.

Mentions: Bcl-2, Bax and caspase 3 expression were observed by immunohistochemical staining in the ischemic cortex (supplementary Figure 2 online). As shown in Figure 5, Bcl-2 protein expression was significantly reduced in the ischemia/reperfusion group compared with the sham-surgery group rats (P < 0.01). Bcl-2 protein expression was significantly restored by IPost and ischemic preconditioning treatment, whereas Bax and caspase 3 expression increased significantly in the ischemia/reperfusion group when compared with the sham-surgery group, both of which were attenuated by IPost and ischemic preconditioning treatment (P < 0.01).


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 influenced the expression of apoptosis-related proteins.Immunostaining for Bcl-2, Bax, and caspase-3. Each bar represents the mean ± SD of quadruplicate studies. aP < 0.01, vs. I/R group. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test.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 5: IPost influenced the expression of apoptosis-related proteins.Immunostaining for Bcl-2, Bax, and caspase-3. Each bar represents the mean ± SD of quadruplicate studies. aP < 0.01, vs. I/R group. Different groups were compared by one-way analysis of variance and the Student-Newman-Keuls test.I/R: Ischemia/reperfusion; IPost: ischemic postconditioning; IPC: ischemic preconditioning.
Mentions: Bcl-2, Bax and caspase 3 expression were observed by immunohistochemical staining in the ischemic cortex (supplementary Figure 2 online). As shown in Figure 5, Bcl-2 protein expression was significantly reduced in the ischemia/reperfusion group compared with the sham-surgery group rats (P < 0.01). Bcl-2 protein expression was significantly restored by IPost and ischemic preconditioning treatment, whereas Bax and caspase 3 expression increased significantly in the ischemia/reperfusion group when compared with the sham-surgery group, both of which were attenuated by IPost and ischemic preconditioning treatment (P < 0.01).

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