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- Title
AMPK mediated up-regulaiion of Bim involved in early coriical apoptosis after subarachnoid hemorrhage in rats.
- Authors
AN Ji-yang; ZHOU Li-li; SONG Jin-ning; LUO Xian-hua; CHENG Mao-feng; SUN Peng; PANG Hong-gang
- Abstract
Objective To investigate the activation of AMP-activated protein kinase (AMPK) and Bim in rat cortex after subarachnoid hemorrhage (SAH) and to explore the role of AMPK in cortical apoptosis in early brain injury after SAH. Methods SAH model was established by an endovascular perforation technique. The immunohistochemical method was used to detect the localization of AMPK and phosphorylated AMPK. RT-PCR was performed to detect the dynamic mRNA expression of AMPKα, and Western blot was used to detect the protein leveis of phosphorylated AMPK and apoptosis-related proteins (Bim and caspase-3) in the cortex. After AICAR and compound C were administered via i. c. v, the change of p-AMPK level was examined, and the effects of AICAR and compound C on neurological behavior and apoptosis-related protein expressions were observed. Results Experimental SAH increased the expressions of AMPKα mRNA and phosphorylated AMPK. Bim and caspase-3 were also significantiy increased. Wth compound C treatment, the phosphorylation level of AMPK and the up-regulation of Bim were modfied. However, AICAR administration exacerbated cortical apoptosis and neurological deficit through up-regulation of Bim. Conclusion AMPK is involved in the pathophysiological process of neuronal apoptosis in early brain injury after SAH. The mechanism may be related to the regulation of transcription of Bim. Inhibition of AMPK signaling pathway can provide neuroprotection by reducing cortical apoptosis after SAH.
- Subjects
ADENOSINE monophosphate; PROTEIN kinases; LABORATORY rats; SUBARACHNOID hemorrhage; APOPTOSIS; REVERSE transcriptase polymerase chain reaction
- Publication
Journal of Xi'an Jiaotong University (Medical Sciences), 2013, Vol 34, Issue 6, p704
- ISSN
1671-8259
- Publication type
Article
- DOI
10.7652/jdyxb201306002