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Effect of Adenosine A2A Receptor Knockout on the Expression of cyt C in Partial Cerebral Tissues After HIBD in Neonatal Mice
Ren Suwei1, Gao Yong1, Zhou Dingfu1, Fan Hailing1, Chen Jiangfan2, Wang Xiaotong1, Chen Xiang1*
1Department of Rehabilitation, the Second Affiliated Hospital of Wenzhou Medical College, Wenzhou 325027, China; 2Boston University School of Medicine, Boston 02215, USA
Abstract: The role of adenosine A2A receptor (A2AR)， an important subtype of adenosine receptors， in neonatal mice after hypoxia-ischemia brain damage (HIBD) is still controversial. Studies about the mechanism of A2AR in HIBD will contribute to the clinical treatment of neonatal hypoxia-ischemia encephalopathy (HIE). Our experiment observed the effect of A2AR knockout mice on neurological behavior. We used TUNEL assay combined with HE staining to detect neuronal apoptosis， also we used immunohistochemical assay to detect the expression of active caspase 3 and cytosolic cyt C after HIBD in neonatal mice. In our study， we found that A2AR knockout damaged neurobehavioral function of neonatal mice and increased the expression of apoptotic neuron， active caspase 3 and cytosolic cyt C. The differences of neuronal apoptosis between A2AR knockout mice and wild type mice were significant at 1， 3， 7 d after HIBD in neonatal mice， as well as the differences of active caspase 3 (P<0.01)， while the significant differences of cytosolic cyt C between these two genetypes appeared at 1， 3 d after HIBD (P<0.01). The expressions of cytosolic cyt C and neuronal apoptosis were positively related， as well as the expressions of cytosolic cyt C and active caspase 3. This prompted that A2AR knockout possibly increased neuronal apoptosis by promoting cyt C released into the cytosolic after HIBD in neonatal mice.
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