Xu J, Xu F, Wang R, Seagrave Jc, Lin Y, March T H
Pathophysiology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA.
Exp Lung Res. 2007 Jun-Jul;33(5):197-215. doi: 10.1080/01902140701459514.
The authors tested whether macrophage metalloelastase (MMP-12) and substance P (SP) were increased in the cigarette smoke (CS)-exposed female C3H/HeN mice with hypercapnic emphysema. The authors found that as compared to control (filtered air), 16 weeks of CS exposure significantly up-regulated mRNA and protein levels of MMP-12, the ratio of MMP-12/tissue inhibitor of matrix metalloproteinase-1, and SP/preprotachykinin-A (a precursor to SP) in the lungs. Importantly, a significant correlation was found between MMP-12 and SP, and between MMP-12/SP and the degrees of hypoxemia/hypercapnia denoted in CS-exposed mice. These data suggest a possible involvement of SP and MMP-12 in the pathogenesis of severe COPD.
作者测试了在暴露于香烟烟雾（CS）的患有高碳酸血症性肺气肿的雌性C3H/HeN小鼠中，巨噬细胞金属弹性蛋白酶（MMP-12）和P物质（SP）是否增加。作者发现，与对照组（过滤空气）相比，16周的CS暴露显著上调了肺中MMP-12的mRNA和蛋白质水平、MMP-12/基质金属蛋白酶组织抑制剂-1的比值以及SP/前速激肽原A（SP的前体）。重要的是，在MMP-12与SP之间，以及MMP-12/SP与CS暴露小鼠中所表现出的低氧血症/高碳酸血症程度之间发现了显著相关性。这些数据表明SP和MMP-12可能参与了重度慢性阻塞性肺疾病的发病机制。
