Dygai A M, Skurikhin E G, Pershina O V, Stepanova I E, Khmelevskaya E S, Ermakova N N, Reztsova A M, Krupin V A, Reikhart D V, Goldberg V E
E. D. Goldberg Research Institute of Pharmacology, Siberian Division of the Russian Academy of Medical Sciences, Tomsk, Russia.
Bull Exp Biol Med. 2014 Nov;158(1):21-6. doi: 10.1007/s10517-014-2682-y. Epub 2014 Nov 19.
We studied the effect of ketanserin on hemopoietic progenitor cells (Lin(-)Sca-1(+)c-Kit(+)CD34- and Lin(-)Sca-1(+)c-Kit(+)CD34(+)), progenitor hemopoietic cells (Lin(-)Sca-1(+)c-kit(+)), and multipotent mesenchymal stromal cells (CD45(-)CD73(+)CD106(+)) in C57Bl/6 mice during pulmonary fibrosis. It was shown that the blocker of 5-HT2A receptors lowers the activity of bleomycin-induced inflammation in the lungs and prevents the infiltration of alveolar interstitium and alveolar ducts by hemopoietic stem and hemopoietic progenitor cells; in this case, they are more numerous in the bone marrow of sick animals. Ketanserin reduces the capacity for self-renewal of lung multipotent mesenchymal stromal cells in the fibrotic phase of the disease and inhibits their differentiation into stromal cell lines (adipocytes, chondrocytes, and fibroblasts) simultaneously with the decrease in the percentage of connective tissue in the lung parenchyma.
我们研究了酮色林对C57Bl/6小鼠肺纤维化过程中造血祖细胞(Lin(-)Sca-1(+)c-Kit(+)CD34-和Lin(-)Sca-1(+)c-Kit(+)CD34(+))、造血前体细胞(Lin(-)Sca-1(+)c-kit(+))和多能间充质基质细胞(CD45(-)CD73(+)CD106(+))的影响。结果表明,5-HT2A受体阻滞剂可降低博来霉素诱导的肺部炎症活性,并防止造血干细胞和造血祖细胞浸润肺泡间质和肺泡导管;在这种情况下,患病动物骨髓中的这些细胞数量更多。酮色林降低了疾病纤维化阶段肺多能间充质基质细胞的自我更新能力,并抑制其分化为基质细胞系(脂肪细胞、软骨细胞和成纤维细胞),同时肺实质中结缔组织的百分比也降低。