氧化苦参碱对人瘢痕成纤维细胞前胶原及纤维粘连蛋白表达的影响

目的 研究氧化苦参碱(oxymatrine，OM)对人病理性瘢痕成纤维细胞Ⅰ、Ⅲ型前胶原(procollagen Ⅰ， Ⅲ， PCⅠ， PCⅢ)、纤维粘连蛋白(fibronectin，FN)及基质金属蛋白酶-1(matrix metalloproteinase，MMP-1)表达的作用，并与瘢痕治疗常规药物氢化可的松(hydrocortisone，HC)进行比较。方法 采用组织块培养法培养原代瘢痕疙瘩成纤维细胞(keloid fibroblast，KFb)、增生性瘢痕成纤维细胞(hyperplastic scar fibroblast，HFb)和正常皮肤成纤维细胞(normal fibroblast，NFb)，分别使用OM (500 μg/mL)、HC(2 μg/mL)作用于KFb、HFb和NFb，RT-PCR法检测3种成纤维细胞PCⅠ、PCⅢ、FN及MMP-1 mRNA表达及其药物干预后的变化。结果 正常条件下，与NFb比较，KFb、HFb的PCⅠ mRNA表达分别增加31.7%和34.2% (均P<0.05)，且KFb的PCⅢ mRNA表达增加44.9%(P<0.01)。药物干预后，OM使HFb的FN及PCⅠ mRNA表达量分别减少18.8%和23.6%(均P<0.05)；HC使HFb的FN及PCⅠ mRNA表达量分别减少26.8%和43.6%(P<0.05，P<0.01)；OM还使KFb的MMP-1 mRNA表达量增加21.8%(P<0.05)。结论 OM可能通过抑制病理性瘢痕成纤维细胞PCⅠ和FN mRNA表达而减少细胞外基质(extracellular matrix，ECM)的合成；与HC比较，OM还可通过诱导KFb的MMP-1 mRNA表达增加以促进ECM的降解，因而具有潜在的治疗病理性瘢痕的作用。

Effects of Oxymatrine on the Expressions of Pro-collagen and Fibronectin of Fibroblasts Derived from Human Hyperplastic Scars

Objective To study the effects of oxymatrine (OM) on the expressions of pro-collagen Ⅰ (PC Ⅰ), pro-collagen Ⅲ (PCⅢ), fibronectin (FN), matrix metalloproteinase-1 (MMP-1) mRNA of fibroblasts from keloid (KFb), hyperplastic scar (HFb), and normal skin (NFb), and to compare with hydrocortisone (HC). Methods The primary KFb, HFb and NFb were derived from patients and cultured in vitro using tissue block culture method. The fibroblasts were treated with 500 μg/mL OM, 2 μg/mL HC, or without any medicine (as the control). The mRNA expressions of PCⅠ, PCⅢ, FN, MMP-1 of the fibroblasts were detected using RT-PCR. Results Under the normal condition, when compared with NFb, the mRNA expressions of PCⅠof KFb and HFb increased by 31.7% and 34.2% (both P<0.05). Besides, the mRNA expression of PCⅢ of KFb increased by 44.9% (P<0.01). OM down-regulated the mRNA expressions of FN and PCⅠ of HFb by 18.8% and 23.6% respectively (both P<0.05). HC decreased the mRNA expressions of FN and PCⅠ of HFb by 26.8% and 43.6% respectively (P<0.05, P<0.01). Meantime, OM up-regulated the mRNA expression of MMP-1 of KFb by 21.8% (P<0.05). Conclusions OM suppressed the synthesis of extracellular matrix (ECM) possibly through down-regulating the mRNA expressions of PCⅠ and FN. Compared with HC, OM could promote the degradation of ECM through inducing the MMP-1 mRNA expressions of KFb. Therefore, OM could be potentially used in treatment of hypertrophic scar and keloid.