进口原代小气道上皮细胞培养基

气道上皮细胞培养基是为正常人类气道上皮细胞体外培养设计的适于其生长的培养基。培养基是无菌的、液体培养基，包含必需和非必需氨基、维生素、有机和无机化合物、激素、生长因子、微量矿物质。该培养基不含血清。该培养基含HEPES和碳酸氢盐缓冲体系，在5%二氧化碳/95%空气培养箱中平衡时PH值为7.4。该培养基在数量上和质量上都保证理想的营养平衡状态，选择性促进体外正常人类气道上皮细胞的生长。
  气道上皮细胞培养基包含500 ml基础培养基，5 ml气道上皮细胞生长添加物，(SAEpiCGS,目录编号3272)和5 ml青霉素/链霉素溶液(P/S,目录编号0503)

1. Saux CJL, Davy P, Brampton C, Ahuja SS, Fauce S, Shivshankar P, Nguyen H, Ramaseshan M, Tressler R, Pirot Z, Harley CB, Allsopp R. (2013) "A novel telomerase activator suppresses lung damage in a murine model of idiopathic pulmonary fibrosis." PLoS One. 8: e58423.

The emergence of diseases associated with telomere dysfunction, including AIDS, aplastic anemia and pulmonary fibrosis, has bolstered interest in telomerase activators. We report identification of a new small molecule activator, GRN510, with activity ex vivo and in vivo. Using a novel mouse model, we tested the potential of GRN510 to limit fibrosis induced by bleomycin in mTERT heterozygous mice. Treatment with GRN510 at 10 mg/kg/day activated telomerase 2-4 fold both in hematopoietic progenitors ex vivo and in bone marrow and lung tissue in vivo, respectively. Telomerase activation was countered by co-treatment with Imetelstat (GRN163L), a potent telomerase inhibitor. In this model of bleomycin-induced fibrosis, treatment with GRN510 suppressed the development of fibrosis and accumulation of senescent cells in the lung via a mechanism dependent upon telomerase activation. Treatment of small airway epithelial cells (SAEC) or lung fibroblasts ex vivo with GRN510 revealed telomerase activating and replicative lifespan promoting effects only in the SAEC, suggesting that the mechanism accounting for the protective effects of GRN510 against induced lung fibrosis involves specific types of lung cells. Together, these results support the use of small molecule activators of telomerase in therapies to treat idiopathic pulmonary fibrosis. Less