Expression of Translocator Protein in Early Brain Injury After Subarachnoid Hemorrhage in Mice

ZHOU Jian, GU Long, PENG Jian-hua, PANG Jin-wei, XIE Yu-ke, GUO Ke-cheng, ZHANG Li-fang, ZHANG Xian-hui, CHEN

Abstract

To evaluate the expression of translocator protein (TSPO) in brain tissue within 72 h after subarachnoid hemorrhage (SAH) in mice.  Methods  Forty-four C57BL/6J mice were randomly divided into two groups, 17 in the Sham group and 27 in the SAH group. SAH mice model was performed by endovascular perforation as previously described with slight modifications. Sham group mice were performed by the same method but without piercing the blood vessels. Before and 6 h, 24 h, 48 h, 72 h after modeling, the two groups were scored with modified Garcia score for neurological function. At 6 h, 24 h, 48 h, 72 h after modeling, the mice were sacrificed. Sham group mice were sacrificed at 24 h after modeling. The expression of TSPO in brain tissue was evaluated by Western blot, positron emission tomography-computed tomography (PET-CT) and immunofluorescence staining. Fluorescent double staining was used to assess the relationship of TSPO and microglia.  Results  The neurological function scores of the SAH group mice decreased with time and then increased. The expression of TSPO in the brain tissue increased first and then decreased with time, and there was a negative correlation between them (r=-0.615 6, P < 0.01). PET-CT showed that the tracer intake of mouse brain tissue after SAH was higher than that of Sham group, and the difference was statistically significant (P < 0.05). Immunofluorescence staining showed that TSPO increased in the parietal cortex and basal cortex of the SAH group. And fluorescent double staining suggested that TSPO colocalized with Iba-1 which was a specific marker of microglia.  Conclusion  In the early brain injury after SAH, the expression of TSPO in brain is widely increased, and the expression level increases first and then decreases. TSPO could participate in the activation of microglia and regulate the occurrence and development of brain injury after SAH.

 

Keywords: Subarachnoid hemorrhage, Early brain injury, Translocator protein, Molecular imaging

 

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References


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