【摘要】 目的　探讨丹参治疗系统性硬皮病的药理机制。方法　用四甲基偶氮唑盐 (MTT)方法和光度检测法测定了丹参对成纤维细胞增殖和培养基中胶原含量的影响。结果　丹参水溶性提取物丹参注射液 (10 m g/m l、7.5 m g/ml、 5 .0 m g/m l、2 .5 m g/ml)及其活性单体丹参素 (6 0 μg/m l、 45 μg/ml、 30 μg/m l、15 μg/m l)和原儿茶醛 (40 μg/m l、2 0 μg/m l、10 μg/m l、5 μg/m l) ,以及丹参脂溶性总提取物 (1mg/m l、0 .5 m g/m l、0 .2 5 m g/m l)及其活性单体丹参酮 A (4μg/ml,2μg/m l) ,不仅对患者皮肤成纤维细胞的增殖具有显著的抑制作用 ,还能显著降低该细胞培养基中可溶性胶原的含量 (P<0 .0 5～ 0 .0 1)。上述抑制作用随药物浓度的增高或作用时间的延长而增强。采用流式细胞仪对该细胞周期的检测显示 ,丹参素组 G0 /G1 期细胞 ,原儿茶醛组和丹参酮 A组 G2 + M期细胞的比例较正常人对照组细胞显著增高 (P<0 .0 1)。结论　丹参对体外培养的系统性硬皮病患者的皮肤成纤维细胞的增殖和胶原合成具有显著的抑制作用 ,可能是其治疗系统性硬皮病的药理机理之一。更多还原

【Abstract】 Objective To study the pharm acologic m echanism of Salvia m iltiorrhiza Bunge(SMB) in the treatm ent of system ic scleroderm a(SSc) . Methods We used the cultured SSc skin fibroblasts as an experim ental model and detected the effects of SMB both on the cell proliferation by MTT assay and on the collagen production in the culture m edium by photom etric determ ination.Results The results showed that the SMB water soluble extracts,such as SMB injection (10 m g/ m l、7.5 mg/ m l、 5 m g/ m l、2 . 5 mg/ ml) and its effective m onom er Danshensu (6 0 μg/ m l、45 μg/ m l、30 μg/ m l、15 μg/ m l) and protocate chualdehyde (40μg/ m l、 2 0μg/ ml、 10μg/ m l、 5μg/ m l) ,as well as SMB total liposoluble extract (1mg/ ml、0 .5 mg/ m l、0 .2 5 m g/ m l) and its effective monom er tanshinone A(4μg/ m l、2 μg/ m l) ,could not only significantly inhibit the proliferation of the cultured SSc skin fibroblasts,but also significantly reduce the soluble collagen production in the culture m edium(P<0 .0 5～ 0 . 0 1) .The inhibiting effect was in- creased along with the increasing the concentration of the drugs or the prolonging the time of action. The cell cycle determ ination by flow cytom eter(F CM) analysis showed that the cell proportion in G0 / G1phas- es after treated by Danshensu and in G 2 + M phases by protocate chualdehyde and tanshinone A in- creased significantly than the controls(P<0 .0 1) .Conclusion The above results dem onstrated that SMB could significantly inhibit the proliferation and the collagen synthesis in cultured SSc skin fibroblasts and this m aybe one of its pharm acologic m echanism in the treatm ent of SSc.更多还原