Angiogenesis is a physiological procedure during which the new blood vessels develop from the pre-existing vessels. Uncontrolled angiogenesis is related to various diseases including cancers. Clinical inhibition of undesired angiogenesis is still under investigation. We utilized nicotinic acid, a family member of the B-vitamin niacin (vitamin B3) that has been used in the prevention and treatment of atherosclerosis or other lipid-metabolic disorders, to treat human umbilical vein endothelial cells (HUVECs) and chick chorioallantoic membrane (CAM), and investigated its influence on angiogenesis in vitro and in vivo. We found that nicotinic acid could obviously inhibit HUVEC proliferation induced by vascular endothelial growth factor. Both the in vitro and in vivo assays showed that nicotinic acid could significantly inhibit the process of angiogenesis. To further investigate the mechanism underlying the effect of nicotinic acid on angiogenesis, we found that it might function via regulating the cytoskeleton arrangements, especially the rearranging the structures of F-actin and paxillin. In summary, we discovered that nicotinic acid could obviously inhibit the process of angiogenesis by changing the angiogenesis factor expression levels and inducing the cytoskeleton rearrangement of endothelial cells.

血管生成是一种生理过程，在此过程中新血管从先前存在的血管中发育出来。不受控制的血管生成与包括癌症在内的各种疾病有关。不良血管生成的临床抑制作用仍在研究中。我们利用烟酸（一种已被用于预防和治疗动脉粥样硬化或其他脂质代谢性疾病的B-维生素烟酸（维生素B3）的家族成员）来治疗人脐静脉内皮细胞（HUVEC）和鸡绒膜尿囊膜（CAM），并在体外和体内研究其对血管生成的影响。我们发现烟酸可以明显抑制血管内皮生长因子诱导的HUVEC增殖。无论是在体外和体内试验表明，烟酸可显着抑制血管生成过程。为了进一步研究烟酸对血管生成的影响的机制，我们发现它可能通过调节细胞骨架排列，特别是重新排列F-肌动蛋白和paxillin的结构来发挥作用。总之，我们发现烟酸可以通过改变血管生成因子的表达水平并诱导内皮细胞的细胞骨架重排而明显抑制血管生成的过程。