中文摘要：

目的研究姜黄素诱导增生性瘢痕成纤维细胞凋亡及其分子机制。方法用10、20、40μmol/L姜黄素（对照组0μmol/L）处理增生性瘢痕成纤维细胞24 h,MTT法检测姜黄素对细胞增殖的影响,Annexin V-FITC/PI双标法检测细胞凋亡率,分光光度法检测Caspase-9、Caspase-3活性,Western Blot法检测Bcl-2、Bax蛋白表达。结果 MTT结果显示姜黄素对增生性瘢痕成纤维细胞具有抑制作用,抑制率随姜黄素浓度增加而上升（P〈0.05）;Annexin V-FITC/PI双标法结果显示成纤维细胞凋亡率随姜黄素浓度增加而上升（P〈0.05）;经姜黄素作用,Caspase-9、Caspase-3的活性随姜黄素浓度增加而升高（P〈0.05）;Western Blot结果显示Bcl-2蛋白表达下降,Bax蛋白表达升高,Bax/Bcl-2比值增大,差异有统计学意义（P〈0.05）。结论姜黄素对增生性瘢痕成纤维细胞有抑制增殖和诱导凋亡的作用,其机制与下调Bcl-2蛋白表达、上调Bax蛋白表达,升高Caspase-9、Caspase-3活性有关。

英文摘要：

Objective To investigate the effects of curcumin on cell apoptosis in hypertrophic scar fibroblasts and the related mechanism. Methods The hypertrophic scar fibroblasts were treated with curcumin of 10 p, mol/L, 20 /xmol/L, 40 txmol/L for 24 h. The effects of curcumin on proliferation of hypertrophic scar fibroblasts were detected by MTY assay. The apoptosis rate was analyzed by Annexin V-FITC/PI double staining. The activities of Caspase-9 and Caspase-3 were detected with spectrophotometric method. The protein expression of Bcl-2 and Ban was detected with Western blot assessment. Results MTY assay showed that curcumin could inhibit hypertrophic scar fibroblasts proliferation and the inhibitory rate increased with the concentration of curcumin （P〈0.05）. Annexin V-FITC/PI double staining showed that curcumin could induce apoptosis of fibroblasts and the apoptosis rate which increased with the concentration Of curcumin （P〈0.05）. The activities of Caspase-9 and Caspase-3 were increased with the concentration of curcumin （P〈0.05）. Western Blot assessment showed that curcumin reduced the Bcl-2 protein expression, increased the Bax protein expression and the ratio of Bax/Bcl-2, the differences had the statistical significance （P〈0.05）. Conclusion Curcumin could inhibit proliferation and induce apoptosis of hypertrophic scar fibroblasts. Its mechanism may be associated with increasing the activities of Caspase-3 and Caspase-9 by inhibiting the expression of Bcl-2 protein and promoting the expression of Bax protein.