Abstract:

Objective To explore the effects of M1 polarization of microglia on secondary damage in the thalamus after cerebral cortical infarction. Methods A focal cortical infarct model of adult male SD rats was prepared using eletrocoagulation and randomized into Sham and model groups at different time points 1 ~ 4 weeks after surgery. Based on the assessment of neurofunctional changes in each group of rats， immunohistochemistry was used to observe the number and morphology of NeuN， GFAP and Iba-1 positive cells in （Ventral posterior nucleus of thalamus， VPN） of the ipsilateral thalamus after distal middle cerebral artery occlusion （dMCAO）. Immunofurescence was used to detect the number and morphology of M1 microglia marker （Iba-1⁺/CD68⁺ cells） and M2 microglia marker （Iba-1⁺/CD206⁺ cells） in VPN of the ipsilateral thalamus after dMCAO. Western blot was used to detect the expression levels of IL-1β， TNF-α， IL-10 and Arg-1 in VPN of the ipsilateral thalamus after dMCAO. Results The results of immunohistochemistry showed a significant decrease in NeuN positive cells and an increase in the density of GFAP and Iba-1 in the ipsilateral VPN of rats after dMCAO when compared with Sham group （P < 0.001）. Compared with sham group， the protein levels of TNFα and IL-1β were elevated in the ipsilateral VPN elevated （P < 0.05）. In addition， the model group rats exhibited higher Bederson scores， beam-walking test and adhesive removal test scores after dMCAO compared with Sham group （P < 0.05）. The numbers of M1 microglia marker （Iba-1⁺/CD68⁺ cells） were significantly increased when compared with M2 microglia marker （Iba-1⁺/CD206⁺ cells） in ipsilateral VPN of rats after dMCAO. Conclusion M1 polarization of microglia may play an essential role in secondary damage of thalamus after cerebral cortical infarction.

Key words: cerebral infarction, secondary damage, thalamus, microglia polarization, neuroinflammation