《中国康复理论与实践》 ›› 1999, Vol. 5 ›› Issue (01): 6-8.

• 理论与实践 • 上一篇    下一篇

肥厚性瘢痕胶原降解的研究

吴宗耀; 武继祥; 刘宏亮; 汪琴; 尹清; 王德怀   

  1. 第三军医大学西南医院康复理疗科
  • 收稿日期:1998-07-15 出版日期:1999-03-25 发布日期:1999-03-25

A Study on the Catabolism Degradation of Collagen in Hypertrophic Scar

Wu Zongyao,Wu Jixiang,Liu Hongliang,et al   

  1. Chinese Journal of Rehabilitation Theory & Practice.-1999,5(1):6~8
  • Received:1998-07-15 Published:1999-03-25 Online:1999-03-25

摘要: 目的:研究肥厚性瘢痕中胶原累积和清除两方面的相对关系。方法:实验方法有临床观察、动物模型和细胞培养。观察方法有:光镜与电镜、组织化学、原位杂交、斑点杂交等等。结果:①肥厚性瘢痕的自然形成极慢,而用药物干预可以在一个月以内使其消退1/3~2/3。②肥厚性瘢痕中的胶原合成速度有所增加,但其降解速度减慢更为显著。③肥厚性瘢痕中胶原酶的表达有所增加,但其实际生成量和活性则为降低。④肥厚性瘢痕中Ch-4-S明显增加,一方面包绕胶原纤维,阻碍胶原酶的接触和降解作用,另一方面也通过TIMP降低胶原酶的活性。⑤肥厚性瘢痕中TIMP增加,降低胶原酶的活性。⑥肥厚性瘢痕中TGB-β显著增加,其表达量与TIMP表达成正相关,与凋亡细胞数成负相关。TGF-β使MMP-1表达减少,活性下降。⑦肥厚性瘢痕中的成纤维细胞绝大多数为肌成纤维细胞,增殖期凋亡极少,成熟期显著增多。结论:①肥厚性瘢痕中成纤维细胞凋亡减缓和胶原酶数量和活性降低,胶原被Ch-4-S包绕而降解减慢,以致胶原累积,是肥厚性瘢痕形成的主要方面。②加速细胞凋亡和胶原降解可能是防治肥厚性瘢痕比较容易而快捷的途径。

关键词: 肥厚性瘢痕, 胶原, 降解

Abstract: Purpose: To understand the function of catabolism degradation in the formation and deterioration of hypertrophic scar. Method: The study was carried out clinically, on animal model and cultured fibroblast cell. The investigation was conducted with naked eye, microscope, situ hybridization, dot blot hybridization, TUNEL and immunohistochemistry. Result:①The hypertrophic scar grew up very slow but might be eliminated 1/3 to 2/3 within one month with different chemical intervention. ②The synthesis of collagen in hypertrophic scar increased a little, but it's degradation decreased much more. ③The collagenase MMP-1 could destroy the collagen after local injection into the hypertrophic scar, it was proved by light and electromicroscope. ④The expression of MMP-1 Mrna increased a little in hypertrophic scar, but MMP-1 in the scar really decreased in quantity and activity. ⑤Ch-4-S increased significantly in hypertrophic scar, it wrapped up the collagen fibrils and blocked its contact with and avoided its catabolism by MMP-1.TIMP increased in hypertrophic scar and depressed the activity of MMP-1. ⑦The expression of TGF-β increased significantly. It positively related with the expression of TIMP and negatively related with the apototic phenomena in hypertrophic scar. The fibroblast in hypertrophic scar was rich and active, but its proliferation was not elevated and apotosis was delayed. Conclusion: ①The delay of apotosis of fibroblast, the wrapping of collagen by Ch-4-S, the reduction of collagenase in quantity and activity together made the abolition of collagen decreased and might be primary for the formation of hypertrophic scar. ②Accelerating the apotosis of fibroblast and catabolism of collagen might be an easy and rapid way for prevention and treatment of hypertrophic scar.

Key words: hypertrophic scar, collagen, catabolism degradation