Caspr敲除在蛛网膜下腔出血早期脑损伤机制的实验研究

目的探讨黏连蛋白相关蛋白（Caspr）敲除对小鼠蛛网膜下腔出血（SAH）后早期脑损伤（EBI）的影响及其可能的作用机制。方法采用C57BL/6小鼠及Caspr敲除（Caspr+/-）小鼠，共分为4组：SAH模型组、假手术组、Caspr+/-+SAH模型组和Caspr+/-组，采用视交叉前池注血法建立SAH模型。SAH发生24 h后进行神经功能评分和脑水肿检测。采用Western Blot和ELISA法检测Caspr、B淋巴细胞瘤-2基因（Bcl-2）、Bax、Caspase-1、白细胞介素1β（IL-1β）和IL-18的表达；采用TUNEL染色法观察SAH后神经元的凋亡。结果Caspr敲除导致Bcl-2表达下降，Bax、Caspase-1、IL-1β和IL-18表达升高，促进神经元凋亡。结论Caspr敲除通过激活神经细胞凋亡加重SAH后的EBI。

Objective To explore the effect of contactin-associated protein（Caspr） knockout on early brain injury(EBI) after subarachnoid hemorrhage(SAH) in mice and its possible mechanism of action. Methods C57BL/7 and Caspr+/- mice were randomly divided into four groups including sham group, SAH model group, Caspr+/- group and Caspr+/-+SAH group. SAH model was established by stereotactic injection of autologous blood into the optic chiasm cistern. Neurological score and brain edema was performed at 24 hours after SAH. The expressions of Caspr, B-cell lymphoma-2（Bcl-2）， Bax, Caspase-1, interleukin-1β（IL-1β） and IL-18 were detected by Western blot and ELISA. Neuronal apoptosis after SAH was observed by TUNEL staining. Result Caspr knockout decreased Bcl-2 expression, increased the expression of Bax, Caspase-1, IL-1β and IL-18, and upregulated neuronal apoptosis. Conclusion Caspr Knockout can aggravate the EBI after SAH via activating neuronal apoptosis.