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Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples
Published on: October 23, 2020
A mechanistic investigation into non-infarcted brain injury induced by cerebral artery microemboli
Yiying Wu1, Leisi Bian, Xiushi Ni
1Department of Geriatrics, Shanghai First People's Hospital, Shanghai Jiaotong University, No. 100 Haining Road, Shanghai, 200080, China.
Abstract:
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 μm microemboli in 300 μl 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-α expression was detected by using ELISA and the NF-κB 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-α and NF-κB were significantly increased in the microemboli group (P < 0.001), and the increase of the expression of TNF-α and NF-κB on the 3 days was more significant compared to that of TNF-α and NF-κB on 7 days (P < 0.001). Injection of 25-50 μm microemboli at a dose of 100 microemboli in 300 μl 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-α and NF-κB may play important roles in the pathogenesis of neuronal apoptosis induced by microemboli in the cerebral arteries.
Insights
Microemboli in rat carotid arteries caused neuronal apoptosis and glial activation without infarction. Tumor necrosis factor-alpha (TNF-α) and nuclear factor-kappa B (NF-κB) were implicated in this non-infarct brain injury.
Area of Science:
- Neuroscience
- Pathology
- Cerebrovascular Research
Background:
- Cerebral artery microemboli can cause brain injury.
- Understanding non-infarctional neural injury mechanisms is crucial.
Purpose of the Study:
- To establish a rat model of non-infarctional brain injury induced by cerebral artery microemboli.
- To explore the neural injury mechanisms involved in microemboli-induced brain damage.
Main Methods:
- Rats received injections of microemboli or saline into the carotid artery.
- Neuronal damage, glial activation (microglia and astrocytes), and inflammatory markers (TNF-α, NF-κB) were assessed.
- Histological (HE, caspase-3, CD11b, GFAP) and molecular (ELISA, Western blotting) techniques were employed.
Main Results:
- Microemboli injection did not cause cerebral infarction.
- Significant increases in apoptotic cells and glial activation (CD11b, GFAP) were observed in the microemboli group compared to the sham group.
- Elevated expressions of TNF-α and NF-κB were detected in the microemboli group, with higher levels at 3 days post-operation.
Conclusions:
- Cerebral artery microemboli can induce neuronal apoptosis and glial activation without infarction.
- TNF-α and NF-κB play significant roles in the pathogenesis of microemboli-induced neuronal apoptosis.
