A mechanistic investigation into non-infarcted brain injury induced by cerebral artery microemboli

作者：Wu, Yiying; Bian, Leisi; Ni, Xiushi^*; Ning, Min; Zhao, Yanling; Ling, Rujing

来源：Molecular Biology Reports, 2013, 40(2): 1283-1290.

DOI：10.1007/s11033-012-2171-1

• Microemboli
• Neuronal apoptosis
• Inflammatory response
• Rat model

To establish a rat brain injury by non-infarction process model induced by cerebral artery microemboli which would be used to further explore the neural injury mechanisms of cerebral artery microemboli. Seventy-two Sprague-Dawley rats were randomly divided into the microemboli group and the sham group; 100 25-50 mu m microemboli in 300 mu l or the same amount of saline were injected into the left carotid artery, respectively. The severity of neuron damage was assessed 3 and 7 days after the operation, using haematoxylin-eosin (HE) staining and immunohistochemical staining for caspase-3. Immunohistochemical staining for CD11b and GFAP were used to quantitatively analyse hyperplasia and the activation of microglia and astrocytes. TNF-alpha expression was detected by using ELISA and the NF-kappa B expression was detected by employing Western blotting. The results of HE staining had shown that ischaemic infarct foci were not detected in either the microemboli group or sham group. Only a few apoptotic cells and a few cells with the positive expression of CD11b and GFAP were detected in the sham group. And compared with that of the sham group, the number of apoptotic cells and the positive expression of CD11b and GFAP in the microemboli group were significantly increased (P < 0.001). These parameters were also significantly increased 7 days after the operation compared to rats 3 days after surgery (P < 0.001). The expressions of TNF-alpha and NF-kappa B were significantly increased in the microemboli group (P < 0.001), and the increase of the expression of TNF-alpha and NF-kappa B on the 3 days was more significant compared to that of TNF-alpha and NF-kappa B on 7 days (P < 0.001). Injection of 25-50 mu m microemboli at a dose of 100 microemboli in 300 mu l into the carotid artery of rats did not result in cerebral infarction, but led to neuronal apoptosis, hyperplasia and activation of microglia and astrocytes. This leads us to conclude that TNF-alpha and NF-kappa B may play important roles in the pathogenesis of neuronal apoptosis induced by microemboli in the cerebral arteries.

• 出版日期2013-2
• 单位上海交通大学