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    王凤珍, 王兆红, 夏计划, 周恒才, 拾坤. 吡非尼酮对人椎板切除术后硬膜外瘢痕细胞的作用及机制研究[J]. 徐州医科大学学报, 2020, 40(11): 795-799. DOI: 10.3969/j.issn.2096-3882.2020.11.004
    引用本文: 王凤珍, 王兆红, 夏计划, 周恒才, 拾坤. 吡非尼酮对人椎板切除术后硬膜外瘢痕细胞的作用及机制研究[J]. 徐州医科大学学报, 2020, 40(11): 795-799. DOI: 10.3969/j.issn.2096-3882.2020.11.004
    The effect and mechanism of pirfenidone on scar cells from epidural area after laminectomy[J]. Journal of Xuzhou Medical University, 2020, 40(11): 795-799. DOI: 10.3969/j.issn.2096-3882.2020.11.004
    Citation: The effect and mechanism of pirfenidone on scar cells from epidural area after laminectomy[J]. Journal of Xuzhou Medical University, 2020, 40(11): 795-799. DOI: 10.3969/j.issn.2096-3882.2020.11.004

    吡非尼酮对人椎板切除术后硬膜外瘢痕细胞的作用及机制研究

    The effect and mechanism of pirfenidone on scar cells from epidural area after laminectomy

    • 摘要: 目的 探讨吡非尼酮对人椎板切除术后硬膜外瘢痕细胞的作用及机制.方法 采用体外组织块培养人硬膜外瘢痕细胞并建立细胞系,分别加入不同浓度的吡非尼酮培养,CCK-8法检测细胞活力,细胞划痕法观察细胞迁移,TUNEL法检测细胞凋亡,Western blot分析转化生长因子β1(TGF-β1)、α-平滑肌肌动蛋白(α-SMA)、Ⅰ型胶原蛋白、Smad2、磷酸化的Smad2(phospho-Smad2)、Smad3、磷酸化的Smad3(phospho-Smad3)表达.结果 成功分离培养人硬膜外瘢痕成纤维细胞.吡非尼酮可抑制成纤维细胞的活性(P<0.05),且并未增加成纤维细胞的凋亡(P>0.05).吡非尼酮可抑制细胞的迁移,并抑制α-SMA、Ⅰ型胶原蛋白表达及细胞增殖相关蛋白的表达和磷酸化.结论 吡非尼酮可抑制瘢痕成纤维细胞的活性及迁移,其机制可能是通过抑制TGF-β/Smad通路及肌成纤维细胞转化实现的.

       

      Abstract: ob<x>jective To investigate the effect and mechanism of pirfenidone on the epidural scar cells from epidural area after laminectomy. Methods Tissue block culture was used to culture human epidural scar cells and establish cell lines, and then different concentrations of pirfenidone were added to the cultured cells, Cell viability was measured using cck-8 kit, cell migration was observed by scratch method, cell apoptosis was detected through in situ terminal transferase labeling (TUNEL) staining and the ex<x>pression of TGF-β1, α-SMA, collagen type I, Smad2, phospho-Smad2, Smad3, phospho-Smad3 was measured with western blot. Results Human epidural scar fibroblasts were successfully isolated and cultured. Pirfenidone decreased the activity of fibroblasts (P <0.05), but did not increase the apoptosis of fibroblasts (P> 0.05). Pirfenidone inhibited cell migration and the ex<x>pression of α-SMA, collagen type I protein, Cell proliferation-related proteins and proteins phosphorylation were also inhibit by pirfenidone. Conclusion Pirfenidone inhibit the activity and migration of fibroblasts, and its mechanism may be achieved by inhibiting TGF-β/Smad pathway and myofibroblast transformation

       

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