CAJ | 학술논문

目的：研究人尿道狭窄组织中的成纤维细胞中iNOs、HSP47、MMP-1和MMP-2在放射线作用前后表达的变化。方法取材于人尿道狭窄段的新鲜瘢痕组织，并使用消化法与超速贴壁法分离出瘢痕成纤维细胞，在稳定传代5~6代后，给予5Gy单次铱192γ射线照射后，使用Western-blotting半定量分析照射前后iNOs，HSP47，MMP-1和MMP-2的表达情况。结果人尿道狭窄段的瘢痕成纤维细胞在接受固定安全剂量单次照射后，在24h时，iNOs与HSP47表达降低，MMP-1和MMP-2表达升高；在48h时，iNOs表达升高，HSP47持续表达降低，MMP-1和MMP-2持续表达升高。结论取材于人尿道狭窄瘢痕中的成纤维细胞经放射线照射后的生物学指标iNOs处于调节上游，呈时相上的双向调节机制，处于下游的HSP47的表达受抑制，MMP-1和MMP-2表达受激活，可能在抑制成纤维细胞的增殖、减少胶原的稳定合成和促进细胞外堆积胶原的分解3个方面有效抑制瘢痕增生。
목적：연구인뇨도협착조직중적성섬유세포중iNOs、HSP47、MMP-1화MMP-2재방사선작용전후표체적변화。방법취재우인뇨도협착단적신선반흔조직，병사용소화법여초속첩벽법분리출반흔성섬유세포，재은정전대5~6대후，급여5Gy단차의192γ사선조사후，사용Western-blotting반정량분석조사전후iNOs，HSP47，MMP-1화MMP-2적표체정황。결과인뇨도협착단적반흔성섬유세포재접수고정안전제량단차조사후，재24h시，iNOs여HSP47표체강저，MMP-1화MMP-2표체승고；재48h시，iNOs표체승고，HSP47지속표체강저，MMP-1화MMP-2지속표체승고。결론취재우인뇨도협착반흔중적성섬유세포경방사선조사후적생물학지표iNOs처우조절상유，정시상상적쌍향조절궤제，처우하유적HSP47적표체수억제，MMP-1화MMP-2표체수격활，가능재억제성섬유세포적증식、감소효원적은정합성화촉진세포외퇴적효원적분해3개방면유효억제반흔증생。
Objective To detect the expressions of iNOs, HSP47, MMP-1 and MMP-2 in fibroblasts of urethral stricture tissue expose toγRadiation. Methods Fresh scar tissue of urethral stricture section was collected and the fibroblasts were isolated using the digestion method and speeding adherence method.The isolated cells weresubcultured 5-6 generations and exposed to the radiation with the frequency of 5Gy/1 times. The expression of iNOs, HSP47, MMP-1 and MMP-2 before and after the radiation were measured by western blot. Results Under the single radiation with fixed safety dose, scar fibroblasts had lower expression of iNOs and HSP47, and higherexpression of MMP-1 and MMP-2 at the time of 24h; at the time of 48h, the treated cells had higher expression of iNOs, continuously lower expression of HSP47, and continuously higher expression of MMP-1 and MMP-2. Conclusion The expression of- iNOs in fibroblasts in exposure to radioactive rays presents the time-phase and two-way regulatory mechanism, and the expression of HSP47, at the downstream, is downregulated. The expressions of MMP-1 and MMP- 2 are upregulated, which may effectively inhibit the scar proliferation by inhibiting the proliferation of fibroblasts, reducing the stable synthesis of collagen, and accelerating the decomposition of extracellular accumulation collagen.