摘要
目的观察吲哚-3-甲醇对大鼠损伤动脉内膜增生的影响并探讨可能机制。方法采用球囊扩张方法,建立大鼠颈总动脉损伤模型。20只Sprague-Dawley大鼠,随机分为单纯球囊扩张组(对照组)和球囊扩张+吲哚-3-甲醇治疗组(治疗组),其中治疗组又分为3个亚组,在球囊扩张术后灌胃给予吲哚-3-甲醇7d,剂量分别为12.5、25、50mg/d,2周后取损伤段血管用于病理组织学检查和免疫组化染色检查。结果①治疗组内膜厚度、内膜面积均显著小于对照组(P<0.05);管腔狭窄程度较对照组分别降低25.2%、29.9%、48.5%。②PCNA阳性细胞表达在治疗组明显低于对照组。③各治疗组细胞凋亡率与对照组比较均明显增高(P<0.01)。结论口服适宜剂量吲哚-3-甲醇可抑制血管内膜增生及血管再狭窄,并可能与其抑制平滑肌细胞增殖并诱导其凋亡有关。
Objective To observe of rat artery after balloon injury and the the effects of indole-3-carbinol on possible mechanisms. Methods neointimal hyperplasia and restenosis Balloon dilation was used to establish the neointimal injury model of left carotid artery in rats. Twenty Sprague-Dawley rats were randomly divided into single balloon dilation group (control group) and balloon dilation followed by indole-3-carbinol therapy group ( therapeutic group). After balloon dilation, indole-3-carbinol ( 12.5, 25, 50 mg/d) was applied to the rats for 7 days respectively. The rats were killed two weeks after balloon dilation and the injured vascular specimens were harvested for pathologic examination and immunohistochemical staining. Results (1)The neointimal thickness, neointimal area in the therapeutic groups were significantly less than that of the control group ( P 〈 0.05). The stenosis ratio of vessels in the therapeutic groups decreased by 25.2%, 29.9% and 48.5% respectively, as compared with the control group. (2)The percentages of PCNA positive cells were obviously decreased in the therapeutic groups as compared with the control group. (3)The apoptosis of vascular smooth muscle cells was significantly higher in the therapeutic groups than the control group ( P 〈 0.01 ). Conclusion Taking indole-3-carbinol orally can inhibit neointimal hyperplasia in vivo, which mechanism may be related to inhibiting the proliferation and promoting the apoptosis of vascular smooth muscle cells.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2007年第15期1504-1506,共3页
Journal of Third Military Medical University
关键词
吲哚-3-甲醇
细胞
平滑肌
增殖
凋亡
indole-3-carbinol
cells, smooth muscle
proliferation
apoptosis