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目的观察人arresten重组蛋白对移植物动脉硬化的抑制作用。方法用pRSET原核表达系统表达并纯化人arresten重组蛋白。建立腹主动脉移植大鼠模型,将受体鼠分为同系动脉移植组、异系移植对照组和异系移植实验组。自术后第3天起,皮下给予arresten重组蛋白(每日5 mg/kg体重)处理。8周后取移植动脉组织标本,进行病理组织学观察与免疫组织化学染色,分析移植动脉新生内膜增生及新生内膜细胞α-平滑肌肌动蛋白(α-SMA)和PCNA的表达。结果异系移植组移植动脉新生内膜中α-SMA表达阳性平滑肌细胞大量增生,致动脉内膜增厚,管腔狭窄。异系移植实验组移植动脉内膜增生受到明显抑制,新生内膜面积(0.14±0.03)mm~2及新生内膜/中膜面积比(0.807±0.073)均显著低于异系移植对照组[(0.33±0.07)mm~2,(1.794±0.089),P<0.01];并且异系移植实验组移植动脉新生内膜细胞PCNA标记指数(31.72±5.26)%显著低于异系移植对照组(69.53±4.38)%(P<0.01)。结论人arresten重组蛋白能有效抑制移植物动脉硬化的发生发展,在抗移植物慢性排斥反应方面显示出良好的应用前景。
Objective To observe the inhibitory effect of human arresten recombinant protein on graft arteriosclerosis. Methods Human arresten recombinant protein was expressed and purified from pRSET prokaryotic expression system. A rat model of abdominal aorta transplantation was established, and the recipient mice were divided into three groups: the femoral artery transplantation group, the heterologous transplantation control group and the xenotransplantation experimental group. From day 3 postoperatively, arresten recombinant protein (5 mg / kg body weight daily) was administered subcutaneously. After 8 weeks, the grafted arteries were harvested and histopathologically and immunohistochemically stained for the expression of α-smooth muscle actin (α-SMA) and PCNA in neointimal hyperplasia and neointimal hyperplasia. Results In heterotopic transplantation group, the expression of α-SMA in the neointimal of transplant artery was hyperplastic, and the intimal thickening and stenosis were found. The intimal hyperplasia of allograft transplantation group was significantly inhibited, the neointimal area (0.14 ± 0.03) mm ~ 2 and neointimal / medial area ratio (0.807 ± 0.073) were significantly lower than those in the heterotopic transplantation [ (0.33 ± 0.07) mm ~ 2, (1.794 ± 0.089), P <0.01]. And the number of PCNA labeling index (31.72 ± 5.26)% was significantly lower in allogeneic transplantation group than that in allograft control group 69.53 ± 4.38)% (P <0.01). Conclusions Human arresten recombinant protein can effectively inhibit the occurrence and development of graft atherosclerosis and has good application prospect in the aspect of anti-graft chronic rejection.