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目的：血管紧张素II 2型受体（AT2R）基因转染的骨髓间充质干细胞（MSC）在四环素可调控系统下作为载体，利用计算机图像分析系统研究新生内膜增生的情况，并探讨AT2R在体可调控表达对大鼠颈动脉损伤后骨桥蛋白（OPN）表达影响。方法：利用球囊损伤60 只SD大鼠颈动脉，并随机将SD 大鼠分为5 组，分别为正常组（未行球囊扩张术）、对照组（球囊扩张术后注入 PBS）、MSC 组（球囊扩张术后注入常规MSC）、MSC转染组（球囊扩张术注入转染AT2R的MSC）、强力霉素(Dox)组（球囊扩张术后注入转染AT2R 的MSC，术后当天至处死前三天通过尾静脉注射Dox 100 滋g/kg/d）。术后14 及28 天分别处死大鼠取材，光镜下观察血管内膜增生情况，Image pro plus 6.0 计算机图像分析系统测量新生内膜面积（I/M），逆转录- 多聚酶链反应（RT-PCR）检测AT2R及OPN 在大鼠血管标本中的表达变化。结果：大鼠颈动脉AT2R 在Dox组的表达显著增高，新的增生内膜面积较其它各损伤组显著降低（P≤ 0.01），并且OPN 的表达显著低于其他各手术组。结论：AT2R 基因在体可调控表达受到Dox 的有效控制， AT2R 基因可能抑制血管损伤后OPN的表达及新生内膜的过度增生。

英文摘要:

Objective:To investigate the neointimal hyperplasia status through the carrier of mesenchymal stem cells(MSC) transfected by angiotensin II type 2 receptor(AT2R) which medicated by tetracycline regulatable system, and explore the effect of AT2R regulatable expression on osteopontin(OPN) in rats with injured carotid artery.Methods:A total of 60 SD rats, whose carotid arteries were injured by balloons, were randomly divided into 5 groups: normal group (without undergoing balloon dilatation), control group(injected PBS after balloon dilatation), MSC group (injected MSC after balloon dilatation), MSC transfection group (injected MSC transfected by AT2R after balloon dilatation) and Deoxycycline (Dox) group (injected MSC transfected by AT2R after balloon dilatation, and injected Dox 100 滋g/kg/d fromafter balloon dilatation to three days after death). All the rats were killed during 14 d and 28 d after balloon dilatation, and the eointimal hyperplasia status of the rats was observed under light microscope; the intima/media (I/M) area was measured by image analysis systemof Image pro plus 6.0, and the changes of AT2R and OPN expression were detected by RT-PCR method.Results:The expression of AT2R in Dox group significantly increased and its I/M area significantly decreased compared with other groups (P≤ 0.01), and the OPN expression was lower than other groups.Conclusion:AT2R regulatable expression is effectively controlled by Dox, and AT2R may inhibit OPN expression and excessive neointimal hyperplasia.

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