Regenerative therapy for acute lung injury based on intercellular cross talk

急性肺损伤的再生治疗包括肺泡上皮和上皮细胞的增殖和修复，以及[3]预防肺纤维化。从外周血中分离CD 34阳性细胞，并使用含有VEGF、FBS和IGF的EBM-2培养基分化为上皮祖细胞。在博莱霉素诱导的肺损伤中，而不是内毒素诱导的肺损伤中，血管增殖。咯利普兰（PDE-IV抑制剂）对肺泡II型肺细胞（AEC-II）增殖的影响。Rolipram增加自发增殖和增强KGF/HGF诱导的增殖。BrdU抗体的免疫组化分析显示，咯利普兰增加了KGF/HGE处理的小鼠II型肺细胞的DNA合成。腹腔注射内毒素致小鼠急性肺损伤。咯利普兰可减轻肺损伤的形态学损害。我们还进行了生化和病理学研究，是否外源性肺内滴注从大鼠分离的AEC-II可以防止内毒素诱导的肺损伤的纤维化变化。肠内给药的AEC-Ⅱ细胞减弱了上皮细胞的损伤和肺泡纤维化，但不显着。

Regenerative therapy for acute lung injury consists of proliferation and repairment of alveolar epithelial and epithelial cells, and [3] prevention of lung fibrosis.CD34-positive cells were isolated from peripheral blood, and were differentiated to epithelial progenitor cells using EBM-2 medium containing VEGF, FBS, and IGF. In bleomycin-induced lung injury but not endotoxin-induced lung damage, blood microvessels were proliferated. The effects of rolipram (PDE-IV inhibitor) on proliferation of alveolar type II pneumocytes (AEC-II). Rolipram increased spontaneous proliperation and enhanced KGF/HGF-induced proliferation. Immunohistochemical analysis using BrdU antibody revealed that rolipram increased DNA synthesis in type II pneumocytes in mice treated with KGF/HGE. Acute lung injury was induced by intraperitoneal endotoxin in mice. Rolipram attenuated the morphological damages of the lung injury. We also biochemically and pathologically investigated whether exogenous intratracheal instillation of AEC-II isolated from rats can prevent fibrotic changes in endotoxin-induced lung injury. Intratracheal administration of AEC-II cells attenuated damage of epithelial cells and alveolar fibrosis although not significantly.