论文部分内容阅读
目的对严重急性呼吸综合征(SARS)患者肺组织中基质金属蛋白酶-9(MMP-9)、巨噬细胞(CD68+细胞)及弹性纤维进行定量分析,研究三者之间变化的关系,探讨MMP-9在SARS患者肺损伤修复中的作用机制和意义。方法通过免疫组织化学技术对6例SARS死亡患者肺和5例肺外伤患者手术切除的正常肺组织中MMP-9和CD68+细胞进行检测,Gomori醛品红法显示弹性纤维,应用Motic Advanced 4.0图像分析系统进行定量分析,测定MMP-9的面密度、CD68+细胞的数量、弹性纤维的含量,并与正常对照组进行比较。结果SARS患者肺组织中MMP-9和CD68+细胞的数量均明显增加,而弹性纤维的含量明显减少,提示SARS患者肺组织中弹性纤维出现断裂。相关分析显示,SARS患者肺组织中MMP-9的面密度与CD68+细胞的数量呈正相关,与弹性纤维的含量呈负相关。结论SARS死亡患者肺组织中巨噬细胞的增加可引起MMP-9明显增加,后者可导致弹性纤维的降解,MMP-9在SARS患者肺损伤修复过程中可能起到桥梁作用。
Objective To quantitatively analyze the expression of matrix metalloproteinase-9 (MMP-9), macrophage (CD68 +) cells and elastic fibers in patients with severe acute respiratory syndrome (SARS) -9 in SARS patients with lung injury repair mechanism and significance. Methods Immunohistochemistry was used to detect the MMP-9 and CD68 + cells in 6 cases of SARS-dead lungs and 5 cases of lung trauma patients. The Gomori aldehyde magenta method showed elastic fibers. Motic Advanced 4.0 image analysis System quantitative analysis, determination of the surface density of MMP-9, CD68 + cells, the content of elastic fibers, and compared with the normal control group. Results The numbers of MMP-9 and CD68 + cells in the lung tissue of SARS patients were significantly increased, while the content of elastic fibers was significantly reduced, suggesting that the elastic fibers in the lung tissue of SARS patients were broken. Correlation analysis showed that the surface density of MMP-9 in lung tissue of SARS patients was positively correlated with the number of CD68 + cells and negatively correlated with the content of elastic fibers. Conclusion The increase of macrophages in the lung tissue of SARS patients may cause the increase of MMP-9, which may lead to the degradation of elastic fibers. MMP-9 may play a bridge role in the repair of lung injury in SARS patients.