中文摘要：

目的探讨NADPH氧化酶对培养的小鼠血管平滑肌细胞（vascularsmoothmusclecell，VSMC）Toll样受体4（Toll—likereceptor4，TLR4）介导的炎症表型中的作用。方法分别采用NADPH氧化酶激动剂血小板衍生生长因子-BB（platelet—derivedgrowthfactor—BB，PDGF-BB）和抑制剂夹竹桃麻素（apocynin）处理培养的C57BL／6J和TLR4-/-小鼠胸主动脉VSMC。分别采用荧光探针二氯荧光素双醋酸盐染色法检测VSMC内活性氧（reactiveoxygenspecies，ROS）含量，酶联免疫吸附法检测VSMC白细胞介素（interleukin，IL）-6、IL-1β和肿瘤坏死因子-α（tumornecrosisfactor—α，TNF—α）表达，四甲基偶氮唑蓝染色法和Boyden小室检测VSMC的增殖和迁移。结果PDGF-BB处理可显著增高C57BL／6J和TLR4-VSMC内ROS含量，而夹竹桃麻素可抑制ROS生成。PDGF．BB处理可使C57BL／6JVSMCIL-6[（52．69±3．49）ng／ml对（35．04±2．74）rig／ml，P=0．001]、IL-1B[（79．68±2．33）ng／ml对（62．38±0．54）ng／ml，P=0．000]和TNF-α[（218．35±5．42）ng／ml对（124．74±4．59）ng／ml，P=0．000]表达显著上调，增殖（1．69±0．53对1．04±0．40，P=0．000）和迁移（42．11±4．05对1．69±0．53，P=0．000）能力均显著增强，而夹竹桃麻素预处理则可显著抑制VSMCIL-6[（42．11±4．05）ng／ml对（52．69±3．49）ng／ml，P=0．010]、IL-1B[（67．57±1．36）ng／ml对（79．68±2．33）ng/ml，P=0．000]和TNF-α[（156．18±6．98）ng／ml对（218．35±5．42）ng/ml，P=0．000]表达以及增殖（1．23±0．42对1．69±0．53，P=0．000）和迁移（42．11±4．05对52．69±3．49，P=0．000）。TLR4-VSMC经PDGF—BB和夹竹桃麻素处理后，IL-6、IL-1β和TNF-α表达以及增殖和迁移能力均无显著变化。结论NADPH氧化酶衍生的ROS参与了TLR4介导的VSMC炎症表型以及增殖和迁移，可能是其影响动脉粥样硬化发生和发展的重要机制。

英文摘要：

Objective To investigate the effect of the reduced nicotinamide adenine dinucleotide phosphate （NADPH） oxidase on Toll-like receptor 4 （TLR4）-mediated proinflammatory phenotype of cultured vascular smooth muscle cells （VSMCs） in mice.Methods NADPH oxidase agonist platelet-derived growth factor- BB （PDGF-BB） and inhibitor apocynin were used respectively to treat cultured VSMCs from C57BL/6J and TLR4-/- mice. The fluorescent probe 2＇,7＇-dichlorodihydrofluorescein diacetate was used to detect the reactive oxyen species （ROS） level in VSMCs. An enzyme-linked immunosorbent assay was used to detect the expressions of interletddn （IL）-6, IL-1β, and tumor necrosis factor-α（TNF-α in VSMCs. Tetrazolium blue staining and Boyden chamber assay were used to detect the proliferation and migration of VSMC. Results TheROS levels were increased in VSMCs both from C57BL/6J and TLR4-/- mice after PDGF-BB treatment, and this could be inhibited by apocynin. PDGF-BB pretreatment sigfificantly upregulated the expressions of IL-6 （52. 69±3.49 ng/ml vs. 35. 04 ±2. 74 ng/ml; P =0. 001）, IL-1β （79. 68 ±2. 33 ng/ml vs. 62. 38 ±0. 54 ng/ml; P=0.000）, and TNF-a （218.35± 5.42 ng/mlvs. 124.74±4.59 ng/ml; P= 0.000） in VSMCs from C57BL/6J mice, and the abilities of proliferation （1.69 ± 0. 53 vs. 1.04 ±0. 40; P = 0. 000） and migration （42. 11 ±4. 05 vs. 1.69 ± 0. 53; P = 0. 000） were increased significantly; apocynin pretreatment significantly inhibit the expressions of IL-6 （42. 11 ± 4. 05 ng/ml vs. 52. 69 ± 3.49 ng/ml; P = 0. 010）, IL-1β （67. 57 ± 1.36 ng/ml vs. 79. 68 ±2. 33 ng/ml; P = 0. 000） and TNF-α （156. 18 ±6. 98 ng/ml vs. 218. 35 ± 5.42 ng/ml; P =0. 000）, as well as proliferation （1.23 ±0. 42 vs. 1.69 ±0. 53; P =0. 000） and migration （42. 11 ±4. 05 vs. 52. 69±3.49; P = 0. 000）. While there were no significant changes in the expressions of IL-6, IL-1β, and TNF-α in VSMCs from TLR4 /- mice after PDGF-BB and apocynin pretreatment. Conclusions N