BI-1通过抑制内质网应激诱导的细胞凋亡减轻蛛网膜下腔出血后的早期脑损伤

BI-1 Attenuates Early Brain Injury after Subarachnoid Hemorrhage by Inhibiting Endoplasmic Reticulum Stress-Induced Apoptosis

探讨慢病毒介导BI-1过表达对蛛网膜下腔出血(SAH)后早期脑损伤(EBI)过程中细胞凋亡的影响.BI-1过表达慢病毒溶液侧脑注射后,采用血管内穿刺法建立SAH后EBI大鼠模型.于造模后不同时间点对大鼠进行神经行为学评估.于造模后24h,检测大鼠脑含水量,HE染色观察海马神经元组织形态学变化,TUNEL染色观察海马组织神经元细胞凋亡情况,Western blot检测BI-1蛋白以及内质网应激相关蛋白CHOP、GRP78和Caspase-12的表达情况.实验结果表明,BI-1过表达可减轻SAH后大鼠神经功能障碍、脑水肿程度和神经元细胞的损伤;TUNEL染色结果显示,BI-1过表达可抑制SAH后大鼠神经元细胞的凋亡;Western blot结果表明,SAH可激活内质网应激相关蛋白CHOP、GRP78和Caspase-12的表达,而BI-1过表达却又抑制了SAH后内质网应激相关蛋白的激活.因此,BI-1过表达可通过抑制内质网应激诱导的神经元细胞凋亡,从而减轻蛛网膜下腔出血后的早期脑损伤.

This paper investigates the effect of lentivirus - mediated BI - 1 overexpression onneuronal apoptosis in early brain injury （EBI） after subarachnoid hemorrhage （SAH）. Intravascular puncture method was adopt- ed to establish the SAH model after injected lentiviral solution of BI - 1 overexpression. Neurological assess- ments of rats were performed at different time points after modeling. Twenty four hours after modeling, the brain water content was measured. HE staining was used to observe the histological changes of hippocampal neurons. The apoptosis of hippocampal neurons was detected by TUNEL staining. Western blot was used to an- alyze the protein expression of BI - 1 and endoplasmic reticulum stress -related protein CHOP, GRP78 and