■Sox11,SoxC家族成员之一,是神经发育和神经发生过程中的重要转录因子。然而,目前尚无关于其在神经细胞凋亡中的作用的报道。这项研究旨在检查Sox11在外科脑损伤(SBI)中的功能。
■我们使用90只Sprague-Dawley大鼠建立SBI模型,并使用Sox11的siRNA研究Sox11的作用。蛋白质印迹,实时PCR,免疫荧光,神经元凋亡和坏死,脑水肿,并确定神经评分。
■Sox11的基因和蛋白质数量,与Sham组相比,在SBI之后增加了,在12小时达到峰值。此外,随着siRNA的应用,Sox11蛋白的含量明显少于SBI组。另一方面,神经元凋亡,坏死,脑水肿明显增加,而神经系统评分下降。
■这些发现证明了Sox11在SBI引起的神经损伤后的作用。用siRNA抑制Sox11可能导致神经元损伤和细胞死亡,加重SBI后继发性脑损伤。
UNASSIGNED: Sox11, one of the SoxC family members, is an important transcription factor during neural development and neurogenesis. However, there is no report about its function in neural apoptosis. This research aims to examine the function of
Sox11 in surgical brain injury (SBI).
UNASSIGNED: We used 90 Sprague-Dawley rats to develop the SBI models and the siRNA of
Sox11 to study the roles of
Sox11. Western blot, real-time PCR, immunofluorescence, neuron apoptosis and necrosis, brain edema, and neurological score were determined.
UNASSIGNED: The gene and protein amount of Sox11, compared with the Sham group, were increased after SBI, which reached a peak at 12 hr. In addition, following the application of siRNAs, the amount of
Sox11 protein was significantly less than that in the SBI group. On the other hand, neuronal apoptosis, necrosis, and brain edema were significantly increased, while neurological scores were decreased.
UNASSIGNED: These findings demonstrate the role of Sox11 following nerve injury induced by SBI. Inhibition of Sox11 with siRNA may lead to neuronal injury and cell death, aggravating secondary brain injury after SBI.