Effects of inhibition of adenosine monophosphate -activated protein kinase on expressions of cytochrome c and caspase-3 and neuronal apoptosis in the cerebral cortex after cerebral ischemia-reperfusion injury in mice
10.3760/cma.j.issn.1673-4165.2015.12.004
- VernacularTitle:抑制磷酸腺苷活化蛋白激酶对小鼠脑缺血再灌注后大脑皮质细胞色素c和胱天蛋白酶－3表达及神经细胞凋亡的影响
- Author:
Zhanbo WANG
;
Hua LI
;
Changliang ZHENG
;
Li TAO
;
Shangdong MOU
;
Zhengqi YANG
- Publication Type:Journal Article
- Keywords:
Brain Ischemia;
Reperfusion Injury;
AMP-Activated Protein Kinases;
Apoptosis;
Caspase 3;
Cytochromes c;
Neuroprotective Agents;
Mice
- From:
International Journal of Cerebrovascular Diseases
2015;23(12):899-902
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of inhibition of adenosine monophosphate -activated protein kinase (AMPK) on expressions of cytochrome c (CytC) and caspase -3 and apoptosis in the cerebral cortex after cerebral ischemia-reperfusion injury in mice. Methods Thirty-six male C57BL/6 mice w ere randomly divided into three groups, a sham operation group, a ischemia -reperfusion group, and a AMPK inhibitor group, 12 in each group. A model of middle cerebral artery occlusion w as induced by suture method. The AMPK inhibitor compound C ( 20 mg/kg) w as injected intraperitonealy in the AMPK inhibitor group, the equal volume normal saline w as injected intraperitonealy in the sham operation group and the ischemia-reperfusion group w hen a thread w as inserted. Immunohistochemical staining w as used to detect the expression levels of CytC and caspase-3 and TUNEL method w as used to detect apoptosis at 24 h after ischemia-reperfusion. Results Compared w ith the ischemia-reperfusion group, the numbers of CytC (28.86 ±9.65/HP vs.58.86 ±9.65/HP; t = 7.615, P = 0.030 ) and caspase-3 (7.16 ±5.85/HP vs. 14.36 ±7.85/HP; t =2.548, P =0.035), and TUNEL (67.14 ±8.55/HP vs.95.00 ±13.51/HP; t = 6.891, P = 0.030) positive cels in the cerebral cortex w ere reduced significantly in the AMPK inhibitor group. Conclusion Inhibition of AMPK activity after cerebral ischemia-reperfusion may decrease apoptosis by dow nregulating the expressions of CytC and caspase -3, and play a neuroprotective effect.
