目的 探讨C1q肿瘤坏死因子相关蛋白3（CTRP3）对转化生长因子β1（TGF-β1）诱导的血管外膜成纤维细胞（AFs）增殖以及α-平滑肌肌动蛋白(α-SMA)表达的调节作用。方法 采用细胞贴壁法培养SD大鼠胸主动脉AFs；CCK-8检测不同浓度CTRP3 (0.1、1、10和50 μg/mL) 对AFs增殖的影响；免疫荧光、Real-Time PCR和Western blotting检测CTRP3对AFs α-SMA表达的影响。结果 CTRP3可呈剂量依赖性抑制TGF-β1诱导的AFs增殖，随着浓度升高，其抑制能力增强，浓度为10 μg/mL时，其对AFs增殖的抑制作用最强(P<0.01)；免疫荧光、Real-Time PCR和Western blotting结果显示，CTRP3可明显抑制TGF-β1诱导的α-SMA mRNA和蛋白表达(P<0.01)。结论 CTRP3可在体外抑制TGF-β1诱导AFs的增殖和α-SMA表达，提示其潜在的改善病理性血管重构作用。

Objective To investigate the effects of C1q/TNF-related protein-3 (CTRP3) on transforming growth factor-β1 (TGF-β1) induced proliferation and expression of α-smooth muscle actin (α-SMA) among adventitial fibroblasts (AFs). Methods AFs were isolated from thoracic aortas of male Sprague Dawly (SD) rats. The cells in passage 3 to 5 were treated with various concentrations of CTRP3 (0.1, 1, 10, 50 μg/mL). The effects of CTRP3 on proliferation of AFs were examined by Cell Counting Kit (CCK-8). Immunoflueresence assay, Real-Time PCR, and Western blotting were adopted to detect the expression of α-SMA of AFs. Results CTRP3 attenuated the proliferative activities induced by TGF-β1 in a dose-dependent manner, and the most marked effect could be observed at the concentration of 10 μg/mL (P<0.01). Immunoflueresence assay, Real-Time PCR and Western blotting showed that CTRP3 could significantly inhibited TGF-β1 induced upregulation of α-SMA both at the mRNA and protein levels (P<0.01). Conclusion CTRP3 has significant inhibition effects on proliferation and α-SMA expression of adventitial fibroblasts induced by TGF-β1, which suggests the potential value of CTRP3 in the treatment of pathological vascular remodeling.