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目的观察紫杉醇对同种大鼠移植动脉的影响,探讨紫杉醇对移植物动脉硬化的抑制作用及机制。方法以W istar大鼠为受者,SD大鼠为供者,按供鼠、受鼠不同分为3组,每组8对:同系对照组W istar大鼠接受W istar大鼠的胸腹主动脉移植;同种对照组W istar大鼠接受SD大鼠的胸腹主动脉移植;同种实验组W istar大鼠接受SD大鼠的胸腹主动脉移植,术后1~14 d腹腔注射紫杉醇2 mg.kg-1.d-1。两个对照组每日腹腔注射相同体积的生理盐水。术后30 d,取出移植动脉,进行病理学观察,测出管腔面积和内膜截面积,计算再狭窄率,用免疫组织化学方法测定增殖细胞核抗原(PCNA)的表达。结果同种实验组移植动脉内膜厚度、内膜PCNA表达情况均较同种对照组明显减少,外膜炎症细胞浸润程度、管腔再狭窄率均较同种对照组降低,差异有统计学意义。结论紫杉醇能有效抑制同种大鼠移植动脉内膜增生,防止移植物动脉硬化,其作用机制可能与抑制血管平滑肌细胞增殖和减轻对移植物的免疫排斥反应有关。
Objective To observe the effects of paclitaxel on arterial grafts in rats of the same species and to explore the inhibitory effect and mechanism of paclitaxel on arteriosclerosis. Methods W istar rats were used as donors, SD rats were donors, divided into 3 groups according to donor mice and recipient rats, 8 pairs in each group: Rats in the same control group, W istar, received thoracic and abdominal mass of Wistar rats. Artery transplantation; Wistar rats with the same kind of control group received thoracic-abdominal aorta transplantation in SD rats; Wistar rats with the same experimental group received thoracic-abdominal aortic transplantation of SD rats, and intraperitoneal injection of paclitaxel after 1-14 days after operation. 2 mg.kg-1.d-1. Both control groups were injected intraperitoneally with the same volume of saline daily. At 30 days after surgery, the transplanted artery was removed and pathological observations were performed. The lumen area and the intima-medial cross-sectional area were measured, the restenosis rate was calculated, and the expression of proliferating cell nuclear antigen (PCNA) was measured by immunohistochemistry. Results The intima thickness and endometrium PCNA expression in the same experimental group were significantly lower than those in the same control group. The degree of infiltration of inflammatory cells and the rate of restenosis in the outer membrane were lower than those in the same control group. The difference was statistically significant. . Conclusion Paclitaxel can effectively inhibit arterial intimal hyperplasia and graft arteriosclerosis in allograft rats. The mechanism may be related to inhibiting the proliferation of vascular smooth muscle cells and alleviating the immunological rejection of grafts.