中文摘要：

目的研究炎症因子对类胰岛素样生长因子1（IGF1）沉默表达的人冠状动脉平滑肌细胞（hCASMCs）增殖和凋亡的影响。方法应用慢病毒RNA干扰技术沉默hCASMCs的IGF1表达。分别用未感染病毒载体的细胞和感染阴性对照病毒载体的hCASMCs作为空白对照和阴性对照。肿瘤坏死因子-α50ng／ml与白细胞介素-1β40ng／ml共同刺激细胞8h。采用酶联免疫吸附试验检测细胞培养上清液中IGF1浓度，MTT法及流式细胞术检测细胞的增殖及凋亡。结果炎症因子刺激后，IGF1沉默表达的hCASMCs上清液中IGF1的浓度显著低于空白对照组和阴性对照组[（426．35±120．96）比（1030．69±54．69）和（992．82±26．90）pg／ml，P=0．000]；细胞的增殖活性显著低于两个对照组（0．302±0．011比0．401±0．028和0．393±0．017，F=37．628，P=0．000），凋亡率显著高于对照组[（10．57±0．99）％比（0．19±0．13）％和（1．31±0．30）％，P=0．001]。结论炎症因子可能具有抑制IGF1敲减后的hCASMCs增殖和促进凋亡的作用。

英文摘要：

Objective To study the effect of inflammatory factors on cell proliferation and apoptosis in insulin-like grown factor 1 （IGF1） -slienced human coronary artery smooth muscle cells （hCASMCs） . Methods We silenced the expression of IGF1 in hCASMCs using the lentivirus-mediated RNA interference technology. Blank control group and negative control group were set using the hCASMCs without the infection of a virus vector and the hCASMCs with the infection of a negative control virus vector, respectively. After the treatment of these ceils with both tumor necrosis factor-α 50 ng/ml and inter｜eukin-1 β 40 ng/ml, the concentration of IGF1 in cell-culture medium was detected by enzyme-linked immunosorbent assay, and the proliferation and apoptosis were evaluated by MTT assay and flow cytometry. Results After the simulation with inflammatory factors, the concentration of IGF1 in the supematant fluid of cultured IGFl-slienced hCASMCs was significantly lower than those in the blank control group and negative control group [ （426.35 ± 120. 96） vs. （1 030. 69 ±54. 69） and （992. 82 ± 26. 90 ） pg/ml, P = 0. 000） . The proliferation of IGFl-slienced hCASMCs was substantially much less than the two control groups （0. 302 ± 0. 011 vs. 0. 401 ± 0. 028, and 0. 302 ± 0, 011, F = 37. 628, P = 0. 000）, and the apoptosis rate of IGFl-slienced hCASMCs was significant increased compared with the other two groups [ （10. 57 ±0. 99）% vs. （0. 19 ±0. 13）% and （1. 31 ±0. 30）%, P =0, 001 ] . Conclusion Inflammatory factors can inhibit the cell proliferation and promote apoptosis after the knock-down of IGFI in hCASMCs.