中文摘要：

目的观察缺氧缺血性脑损伤（HIBD）后新生大鼠脑组织中髓鞘抑制因子配对免疫球蛋白B（PirB）的表达变化，以及抑制PirB对缺氧缺血性神经损伤的保护作用。方法66只新生SpragueDawley大鼠随机分为假手术组（n=30）、HIBD组（n=30）和抗PirB抗体组（n=6），采用结扎右侧颈总动脉和低氧（8％O，）处理3h造模，假手术组分离右侧颈总动脉但不予结扎及缺氧处理；HIBD组在完成结扎手术及缺氧处理后，两组分别在0h、6h、12h、24h和72h各处死6只大鼠；抗PirB抗体组在完成结扎手术及缺氧处理后即刻从脑室内注入PirB抗体，于72h后处死。采用免疫组化、Westernblot和RT—PCR方法检测HIBD后各时间点新生鼠脑组织内PirB蛋白及mRNA含量的变化，同时免疫沉淀法测定Rho激酶（ROCK）活性在HIBD72h后的变化以及抗PirB抗体对ROCK活性的影响。结果PirBmRNA和蛋白均在HIBD72h后的新生鼠脑组织中表达升高，与HIBD后0h比较差异均有统计学意义（均P〈0．05）。HIBD后72h，新生鼠脑组织中ROCK蛋白活性高于假手术组和抗PirB抗体组（均P〈0．05）。结论抑制PirB可能是促进HIBD后神经再生的一个新治疗方法，而该抑制作用可能是通过Rho．ROCK信号通路产生的。

英文摘要：

Objective To study changes in paired-immunoglobulin-like receptor B （PirB） expression after hypoxic-ischemic brain damage （HIBD） as well as the role for targeted inhibition of PirB activity in nerve regeneration in rats. Methods Newborn Sprague-Dawleyrats rats were divided into： a sham operation group （n=30）, a HIBD group （n=30）, and an anti PirB antibody treatment group （n=6）. In the HIBD group, HIBD was induced by right carotid artery ligature and subsequent exposure to hypoxia （8% 02） for 3 hours. In the sham operation group, right carotid artery was dissected as in the HIBD group but no ligature and hypoxic exposure was not applied. In the two groups, 6 animals were sacrificed at 0, 6, 12, 24 and 72 hours after the operation and hypoxic exposure. In the antibody treatment group, after Carotid artery ligation and hypoxia exposure as in the HIBD group, an anti PirB antibody was injected intracerebrally and animals were sacrificed 72 hours after the injection. Immediately after sacrifice of the animals at designated time points, brain tissue specimens were collected. The presence and content of PirB protein were assessed by immunohistochemistry and Western blot analysis respectively, the abundance of PirB mRNA was determined by RT- PCR, and the Rho kinase （Rock） activity was determined by immunoprecipitation. Results At 72 hours after operation, PirB mRNA abundance and protein content in the brain were significantly increased as compared with the measurements at 0 hour after operation in the HIBD group （P〈0.05）; ROCK activity was significantly increased in the HIBD group as compared with the sham operation and anti PirB antibody groups （P〈0.05）. Conclusions PirB might be involved in HIBD through a Rho-ROCK-dependent mechanism and antibody-mediated neutralization of PirB in the brain may offer a novel therapeutic strategy for HIBD.