雷公藤内酯醇通过抑制一氧化氮合成酶2表达减缓大鼠移植物血管病的作用
Triptolide ameliorates transplant arteriosclerosis in rat aorta allograft by inhibiting the expression of NO synthase
摘要目的 了解一氧化氮合成酶2(NOS2)在大鼠同种异体移植血管病变中的病理作用以及雷公藤内酯醇对其影响.方法 以Wistar和SD大鼠间的腹主动脉移植为动物模型,实验分同基因组(A组),异基因对照组(B组),异基因雷公藤内酯醇组(C组).于术后7、28、56 d摘取移植动脉,测量移植动脉内膜厚度,并予免疫组织化学染色,观察NOS2在移植血管组织各层的表达,计算各组积分光密度值.结果 术后28、56 d时移植动脉内膜增厚,C组(雷公藤内酯醇组)最高,与A组及B组相比内膜厚度及积分光密度值差异均具有显著性(P<0.05).NOS2的表达在B组表达也最强,C组NOS2表达受到抑制明显弱于B组(P<0.05).结论 雷公藤内酯醇可能通过抑制NOS2的表达减缓移植物血管病的进展.
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abstractsObjective To understand the pathological role of nitric oxide synthase 2 (NOS2) in rat allograft vascular lesions and the effects of triptolide.Methods The abdominal aorta transplantation between Wistar and SD rats was used as an animal model.Three groups were set up..the same genome group (group A),the allogeneic control group (group B),and the isogene Triptolide group (group C).The grafts were removed at 7th,28th,and 56th day after surgery.The transplant artery intima thickness was measured.The irnmunohistochemical staining was applied to observe the NOS2 expression in the vascular tissue layers.The integral optical density value in each group was calculated.Results The arterial intima of transplants at 28th and 56th day postoperation was thickened,and that was thickest in group C among the three groups (P<0.05).There was significant difference in intima thickness and integral optical density between group C with groups A and B (P< 0.05).The expression of NOS2 was strongest in group B,and that in group C was significantly weaker than that in group B (P < 0.05).Conclusion Triptolide is capable of slowing down the progression of graft vascular disease by inhibiting the expression of NOS2.
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