| 朱建熹1 沈术彤2 高丽3 沈伟3 郭军1,2.脑缺血Akt 和MAPK 磷酸酶负性调节c-Jun N 端激酶信号通路[J].,2011,11(11):2018-2021 |
| 脑缺血Akt 和MAPK 磷酸酶负性调节c-Jun N 端激酶信号通路 |
| Relationship Between Akt and MAPK Phosphatase and Activity of c-JunN-terminal Kinase in Rats after Cerebral Ischemia Reperfusion |
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| DOI： |
| 中文关键词: 前脑缺血 JNK Akt MKP |
| 英文关键词: Cerebral ischemia, c-Jun N-terminal kinase, Akt, MKP |
| 基金项目:国家自然科学基金(30871200);南京医科大学科技发展基金重点项目(08NMUZ006) |
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| 中文摘要: |
| 目的：探讨脑缺血再灌后Akt 和MAPK 磷酸酶与JNK 活性下调的关系。方法：采用成年清洁级雄性SD 大鼠，建立四动脉阻
断前脑缺血再灌注模型。缺血10min 后再灌注不同时间（15min, 1h，4h，24h）。侧脑室分别给予PI3K 抑制剂LY294002（LY）和
MAPK 磷酸酶抑制剂放线菌酮(CHO)。免疫印迹观察p-Akt 和p-JNK 蛋白水平变化。结果：脑缺血再灌注4h，JNK 的活性能被Akt
抑制剂LY294002 增强，表明激活的Akt 能够下调JNK 信号通路。而MAPK 磷酸酶抑制剂放线菌酮能上调缺血后JNK 活性，提
示MAPK 磷酸酶通过去磷酸化参与了JNK 的活性抑制。结论：前脑缺血再灌后，激活Akt 和MAPK 磷酸酶参与了JNK 信号通路
负性调节，是抑制JNK 诱导缺血后中枢神经损伤的重要机制。 |
| 英文摘要: |
| Objective: To investigate the relationship between the of c-Jun N-terminal kinase (JNK) pathway and Akt and MKP
Methods: Rats in the experimental group were subjected to four-vessel occlusion method, endured 10 min ischemia followed by reperfusion
for 15min, 1h, 4h and 24h to examine phosphorylation of JNK and its upstream Akt in the rat hippocampi. The PI3K inhibitor LY294002
and MAPK phosphatase inhibitor cycloheximide were administrated to the rat hippocampi to observe the change of JNK activity. Results:
JNK activity at 4h was enhanced obviously, which suggested that activated Akt suppresses the JNK pathway. Moreover, the JNK activity
at 4h was also largely enhanced by cycloheximide, which indicated that the inactivation of JNK by phosphatases occurs at about 4 h via
its dephosphorylation. Conclusion: Both Akt and MAPK phosphatase negatively regulate JNK pathway during cerebral ischemia in rat
hippocampi. |
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