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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。
Objective To investigate the effect of emodin on hypertrophic scar fibroblasts (HSFs) and its mechanism. Methods HSFs were treated with emodin at the final concentrations of 0, 20, 40 and 80μmol·L-1, respectively. The viability of HSFs was determined by MTS assay. Flow cytometry was performed with Annexin V and propidium iodide double staining. blot was used to detect the expression of extracellular signal-regulated kinase 1/2 (ERK1 / 2), phosphorylated protein Bcl-2, myeloid leukemia-1 (Mcl-1) Protein kinase 1 (RIP1) expression. Results Emodin inhibited the proliferation of HSFs in a dose-dependent manner. The mortality rates of HSFs after treated with 40 and 80 μmol·L -1 emodin for 48 h were 28.6% and 68.0%, respectively (P <0.01) , And pan-caspase inhibitor Z-VAD-FMK pretreatment could partially reduce the cell death rate induced by emodin (P <0.05). Emodin could inhibit ERK phosphorylation, Mcl-1 and RIP1 expression. Conclusion Emodin can inhibit the proliferation of HSFs and induce cell death, which may be related to the inhibition of phosphorylation of ERK1 / 2 and the expression of Mcl-1 and RIP1.