目的探讨高血压对新生内膜形成的影响及部分可能机制。方法按双肾双夹法复制易卒中型肾血管性大鼠高血压模型(stroke-prone renovascular hypertensive rats,RHRSP),选取收缩压稳定在180 mm Hg以上、无自发性卒中表现的RHRSP,行左侧颈总动脉内膜剥除术。计算颈总动脉内膜、中膜面积和内膜/中膜面积比率。以抗CD31抗体标记内皮细胞检测再内皮化,以抗α-SMA抗体标记血管平滑肌细胞(vascular smoothmuscle cells,VSMCs),以流式细胞仪检测CXCR4+细胞占总单核细胞的百分比。结果对照正常血压组,高血压组的血压显著增高(203.36±17.31 mm Hg;95.5±10.01 mm Hg,P<0.05,n=20),新生内膜面积增加(2.18±0.11 mm2;1.55±0.14 mm2,P=0.013,n=4),循环中CXCR4+细胞百分比增高(损伤前:30.11%±1.27%;20.91%±2.06%,P=0.019;损伤后7 d:45.64%±3.30%;28.28%±2.56%,P=0.003,n=3～5)。高血压不影响再内皮化,新生内膜的主要成分仍为VSMCs。结论高血压增加血管损伤之前和之后早期循环中的CXCR4+细胞,可能与其促进新生内膜形成有关。
Neurogenesis and angiogenesis play important roles in functional recovery after ischemic stroke. When cerebral ischemia occurs, axon regeneration can compensate for the loss of apoptotic neurons in the ischemic area. The formation of new blood vessels ameliorates the local decrease in blood supply, enhancing the supply of oxygen and nutrients to newly-formed neurons. New blood vessels also act as a scaffold for the migration of neuroblasts to the infarct area after ischemic stroke. In light of this, researchers have been actively searching for methods to treat cerebral infarction. Netrins were first identified as a family of proteins that mediate axon guidance and direct axon migration during embryogenesis. Later studies have revealed other functions of this protein family. In this review, we focus on netrin-1, which has been shown to be involved in axon migration and angiogenesis, which are required for recovery after cerebral ischemia. Thus, therapies targeting netrin-1 may be useful for the treatment of ischemic stroke.
