To investigate the effects of inhibition of adenosine monophosphate-activated protein kinase (AMPK) activity on caspase-3 expression and neuronal apoptosis after cerebral ischemia-reperfusion in mice.

A total of 36 male C57BL/6 mice were randomly divided into a sham operation group, an ischemia-reperfusion group and an AMPK inhibitor group (n=12 in each group). A model of middle cerebral artery occlusion (MCAO) was induced by the suture method. AMPK inhibitor Compound C (20 mg/kg) was injected intraperitoneally while inserting sutures in the AMPK inhibitor group. The equivalent volumes of normal saline solution was injected intraperitoneally at the same time points in the sham operation group and the ischemia-reperfusion group. At 24 h after cerebral ischemia-reperfusion, immunohistochemical staining was use to detect the expression levels of caspase-3. TUNEL method was used to detect neuronal apoptosis in mice.

Compared with the ischemia-reperfusion group, the numbers of the cortical caspase-3 positive cells ( 7.16±5.85 vs. 14.36±7.85; t=2.548, P=0.018) and the TUNEL positive cells (58.86±9.65 vs. 81.00±12.21; t=4.928, P<0.001) per high-power field in the AMPK inhibitor group were decreased significantly.

Inhibition of AMPK activity downregulates the expression of caspase-3 after cerebral ischemia-reperfusion, and reduces neuronal apoptosis.

Brain Ischemia; Reperfusion Injury; AMP-Activated Protein Kinases; Caspase 3; Apoptosis; Mice