经外膜缓释雷公藤内酯醇抑制自体移植静脉内膜增生

目的:探讨经外膜缓释雷公藤内酯醇（triptolide）对自体移植静脉内膜增生的抑制作用。方法:健康雄性新西兰大白兔24只，建立颈外静脉-颈总动脉移植模型。随机将动物等分为3组。空白组移植血管不给任何处理， F-127多聚凝胶对照组在移植血管外膜喷洒20 %F-127多聚凝胶0.5 mL，实验组在移植血管外膜喷洒携带雷公藤内酯醇300μg的F-127多聚凝胶0.5 mL。术后2周取标本。用组织形态学方法检测血管内膜增生程度，免疫组化检测标本中bcl-2和Fas的表达，TUNEL法检测标本中血管平滑肌细胞(VSMC)凋亡的水平。结果:静脉移植2周后，与空白组和F-127对照组比较，实验组血管内膜增生明显受抑制（P<0.05），bcl-2的表达［（18.2±8.4） %］显著减少，而Fas的表达［（21.4±8.9） %］显著增加，凋亡细胞［（28.4±7.6） %］也显著增加（P<0.05）。结论:经外膜缓释雷公藤内酯醇可有效抑制移植静脉内膜增生，这一作用可能系通过促进VSMC凋亡而实现的。

Adventitia applied slow-releasing triptolide inhibits intima hyperplasia in vein graft

Abstract:Objective:To investigate the inhibitory effect of appling slow-releasing triptolide on adventitia on the intima hyperplasia of autologous vein graft.Methods :In 24 male New Zealand rabbits, external jugular vein to common carotid artery models were established, and then were divided into 3 equal groups at random: blank-control group, receiving no management on adventitia of the vein graft; F-127 control group, receiving local application of 0.5 mL of 20 % F-127 on adventitia of the vein graft; experiment group, receiving local application of 0.5 mL of 20 % F-127 containing triptolide 300μg. Vein graft specimens were harvested at 2 weeks after the operation. Histomorphologic methods were used to detect the degree of intima hyperplasia of the specimens. The expression of bcl-2 and Fas of the specimens was detected by immunohistochemistry. The apoptosis vascular smooth muscle cells (VSMC) were detected by TUNEL.Results:Two weeks after vein grafting, compared to blank-control group and F-127 control group, intima hyperplasia of experiment group ［intima thickness （29.9±7.6）μm, I/M 0.56±0.08］ was markedly inhibited (P<0.05). Expression of bcl-2［(18.2±8.4)%］ was reduced significantly, however, expression of Fas(21.4±8.9）% increased markedly, and the apoptotic cells ［(28.4±7.6)%］ also increased markedly (P<0.05).Conclusions:Applied slow-releasing triptolide by F-127 pluronic on the vein graft adventitia can effectively inhibit intima hyperplasia of vein graft by a mechanism of enhancement of VSMC apoptosis.