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背景:转化生长因子-β(TGF-β)是病理性瘢痕形成的重要因素。Smad蛋白家族是近年来发现的TGF-β受体下游信号蛋白。积雪草苷可抑制成纤维细胞增殖及胶原的合成,使瘢痕内的TGF-β表达减少。目的:研究积雪草苷对瘢痕成纤维细胞增殖与磷酸化Smad2和Smad7的作用及机制。设计:以细胞为研究对象,对照、观察性研究。单位:一所大学医院烧伤整形科。对象:实验于2002-04/2003-03在中山大学外科实验室完成。标本取自因增生瘢痕住院进行整形手术的患者6例,男3例,女3例,年龄1～35岁。增生性瘢痕成纤维细胞由本科实验室经原代培养后传代获得。干预:研究分为实验组和对照组,将积雪草苷作用于成纤维细胞为实验组,对照组不加积雪草苷,观察用药前后各指标的改变。主要观察指标:①积雪草苷对磷酸化Smad2和Smad7的影响。②积雪草苷对细胞周期和凋亡的影响。结果:积雪草苷可抑制瘢痕的成纤维细胞从S期进入M期,减少成纤维细胞中磷酸化Smad2的含量,两组差异无显著性意义(t=1.53,P=0.08),细胞中Smad7的含量实验组为(50.80±22.40)%,对照组(32.18±17.84)%,两组的差异有显著性意义(t=2.17,P=0.024)。结论:积雪草苷抑制瘢痕可通过Smad通路发挥作用。
Background: Transforming growth factor-β (TGF-β) is an important factor in pathological scar formation. The Smad protein family is a signaling protein downstream of the TGF-beta receptor discovered in recent years. Asiaticoside can inhibit the proliferation of fibroblasts and the synthesis of collagen, and reduce the expression of TGF-β in scars. Objective: To study the effect and mechanism of asiaticoside on proliferation and phosphorylation of Smad2 and Smad7 in scar fibroblasts. Design: Cells are the subject of study, control, and observational studies. Unit: A university hospital burn and plastics department. Subject: The experiment was performed at the Surgical Laboratory of Sun Yat-sen University from April 2002 to March 2003. Specimens were taken from 6 patients undergoing plastic surgery due to hyperplastic scars, 3 males and 3 females, aged 1 to 35 years. The hypertrophic scar fibroblasts were passaged from the undergraduate laboratory after primary culture. Intervention: The study was divided into experimental group and control group. Asiaticoside was applied to fibroblasts as the experimental group, while the control group was not treated with asiaticoside, and the changes of various indexes before and after the administration of the drug were observed. MAIN OUTCOME MEASURES: 1 Effect of asiaticoside on phosphorylated Smad2 and Smad7. 2 asiaticoside on cell cycle and apoptosis. Results: Asiaticoside inhibited the fibroblasts of scars from entering S phase to M phase, and decreased the content of phosphorylated Smad2 in fibroblasts. There was no significant difference between the two groups (t=1.53, P=0.08). The content of Smad7 was (50.80±22.40)% in the experimental group and (32.18±17.84)% in the control group. There was a significant difference between the two groups (t=2.17, P=0.024). Conclusion: Asiaticoside inhibits scars through the Smad pathway.