Gu Naibing, Dong Yaru, Tian Ye, Di Zhengli, Liu Zhiqin, Chang Mingze, Jia Xiaotao, Qian Yihua, Zhang Weiping
Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 Yanta West Road, Xi'an 710061, China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Xi'an Jiaotong University Health Science Center, 76 Yanta West Road, Xi'an 710061, China; Department of Neurology, Xi'an Central Hospital, Xi'an Jiaotong University School of Medicine, Xi'an 710003, Shaanxi, China.
Department of Neurology, Xi'an Central Hospital, Xi'an Jiaotong University School of Medicine, Xi'an 710003, Shaanxi, China.
Brain Res Bull. 2017 Apr;130:27-35. doi: 10.1016/j.brainresbull.2016.12.006. Epub 2016 Dec 23.
Ischemic stroke is an acute life-threatening disease, which causes neurological dysfunction. The formation of new blood vessels around the infarct is vital to the restoration of perfusion and healing of brain tissue. Studies have shown that intelectin-1 (omentin) promotes endothelial cell function and angiogenesis in response to ischemia and inhibits apoptosis in rats with unilateral hind limb surgery. In the present study, we investigated the neuroprotective role of intelectin-1 following focal cerebral ischemia. We specifically assessed the effect of increased expression of intelectin-1 in promoting angiogenesis and reducing apoptosis. The treatment was administered using a lentiviral vector, 7 days prior to surgery. The surgery was performed using the established middle cerebral artery occlusion (MCAO) model in rats, and the outcome was evaluated 7 days after injury. Our results demonstrated a significant reduction in brain infarction volume following LV-intelectin-1 treatment. Additionally, CD34 and capillary density were increased in the cerebral ischemic penumbra. Real-time PCR and Western blot revealed an increased expression of intelectin-1, and phosphorylation of eNOS and AKT with enhanced expression of bcl-2 in brain tissues. These data suggest that the successful delivery of LV-intelectin-1 ameliorated ischemic brain injury. It promoted endothelial cell function and revasc ularization, and inhibited apoptosis in response to ischemia by stimulating the Akt-eNOS signaling pathway.
缺血性中风是一种危及生命的急性疾病，可导致神经功能障碍。梗死灶周围新血管的形成对于恢复灌注和脑组织愈合至关重要。研究表明，网膜素-1可促进内皮细胞功能以及对缺血的血管生成反应，并抑制单侧后肢手术大鼠的细胞凋亡。在本研究中，我们调查了网膜素-1在局灶性脑缺血后的神经保护作用。我们特别评估了网膜素-1表达增加在促进血管生成和减少细胞凋亡方面的作用。在手术前7天使用慢病毒载体进行治疗。采用已建立的大鼠大脑中动脉闭塞（MCAO）模型进行手术，并在损伤后7天评估结果。我们的结果表明，LV-网膜素-1治疗后脑梗死体积显著减小。此外，脑缺血半暗带中的CD34和毛细血管密度增加。实时PCR和蛋白质印迹显示脑组织中网膜素-1表达增加，eNOS和AKT磷酸化，bcl-2表达增强。这些数据表明，LV-网膜素-1的成功递送改善了缺血性脑损伤。它通过刺激Akt-eNOS信号通路促进内皮细胞功能和血管再生，并抑制对缺血的细胞凋亡。
