中文摘要：

目的探讨大黄素对增生性瘢痕成纤维细胞（HSFs）的作用及其机制。方法分别以终浓度为0,20,40,80μmol·L-1的大黄素处理HSFs,以MTS法检测细胞活力,以Annexin V、碘化丙啶双染法行流式细胞仪检测,以Western blot法检测细胞外信号调节激酶1/2（ERK1/2）及其磷酸化蛋白、B淋巴细胞瘤-2（Bcl-2）、髓样细胞白血病-1（Mcl-1）、受体相互作用蛋白激酶1（RIP1）的表达。结果大黄素对HSFs的增殖活力有抑制作用,且呈剂量依赖性;HSFs在终浓度为40,80μmol·L^-1大黄素作用48 h后死亡率分别为28.6%,68.0%（P〈0.01）,以泛caspase抑制药Z-VAD-FMK预处理能够部分降低大黄素所致细胞死亡率（P〈0.05）;大黄素能够抑制ERK磷酸化、Mcl-1和RIP1的表达。结论大黄素能够抑制HSFs的增殖活力、诱导细胞死亡,其机制可能与其抑制ERK1/2磷酸化及Mcl-1、RIP1蛋白表达有关。

英文摘要：

Objective To investigate the effect of emodin on hypertrophic scar fibroblasts（ HSFs） and explore the underlying mechanism. Methods HSFs were treated by emodin at final concentrations of 0,20,40,and 80 μmol · L^-1,respectively,in the cultural media. Forty-eight hours later,the cells were subjected to MTS assay and flow cytometry assay with annexin V and propidium iodide as dyeing indicators. Whole cell lysates from the cells of every group were subjected to Western blotting to measure the protein expression levels of ERK1 /2,Bcl-2,Mcl-1 and RIP1. Results The cell viability of HSFs was inhibited by emodin in a dose dependent manner. The mortality rate of HSFs treated with emodin for 48 h at the concentrations of40 and 80 μmol· L-1were 28. 6% and 68. 0%,respectively,which was significantly higher than that of the control group（ P〈0. 01）. Pretreatment with Z-VAD-FMK could partially reduce the mortality caused by emodin（ P〈0. 05）. Phosphorylation of ERK1 / 2 and the expression of RIP1 and Mcl-1 were inhibited by emodin. Conclusion Down regulation of ERK1 /2,RIP1 and Mcl-1 by emodin may account for the inhibited proliferation and increased cell death of HSFs.