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Acute lung injury (ALI) is a common, costly and potentially lethal disease with characteristics of alveolar‑capillary membrane disruption, pulmonary edema and impaired gas exchange due to increased apoptosis and pulmonary inflammation. There is no effective and specific therapy for ALI; however, mesenchymal stem cells (MSCs) have been demonstrated to be a potential option. Lipopolysaccharide (LPS) is a highly proinflammatory molecule that is used to mimic an in vivo inflammatory and damaged state in vitro. The present study investigated the effect of bone marrow‑derived MSCs on an LPS‑induced alveolar epithelial cell (A549 cell line) injury and its underlying mechanisms by a Transwell system. It was identified that a high LPS concentration caused a decrease in cell viability, increases in apoptosis, inflammatory cytokine release and NF‑κB activity, disruption of the caspase‑3/Bcl‑2 ratio, upregulation of Toll‑like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and toll‑interleukin‑1 receptor domain‑containing adaptor inducing interferon (TRIF) expression, and facilitation of TLR4/MyD88 and TLR4/TRIF complex formation in A549 cells. Coculture with MSCs attenuated all of these activities induced by LPS in A549 cells. In addition, an increased level of keratinocyte growth factor (KGF) and angiopoietin‑1 (ANGPT1) secretion from MSCs was observed under inflammatory stimulation. KGF and/or ANGPT1 neutralizing antibodies diminished the beneficial effect of MSC conditioned medium. These data suggest that MSCs alleviate inflammatory damage and cellular apoptosis induced by LPS in A549 cells by modulating TLR4 signals. These changes may be partly associated with an increased secretion of KGF and ANGPT1 from MSCs under inflammatory conditions. These data provide the basis for development of MSC‑based therapies for ALI.

To explore CIAPIN1 gene expression in lung carcinoma tissues and its regulatory in the growth of NCI-H446.Fifty-one formalin-fixed paraffin-embedded specimens of primary lung cancer and their non-cancerous counterparts were detected by SABC immunohistochemistry method. Adenoviral vector construction was recombined and the gene was transduced into NCI-H446 cells. The expression of CIAPIN1 protein was identified by Western blot. Trypan blue staining was used to count the alive cells and to draw a cellular growth curve. The changes of cell cycle and apoptosis were analyzed by flow cytometry.The positive rate of CIAPIN1 expression in cancer tissues (39.2%)was much lower than that in non-cancerous counterparts (100%, P0.05). In Ad-CIAPIN1 group, the growth of transfected NCI-H446 cells in vitro was significantly inhibited. In addition the Ad-CIAPIN1-induced cell apoptosis and a predominant arrest in the G1/S phase (P0.01) were observed.The down-regulation of CIAPIN1 expression in tumor is associated with the development of lung carcinoma. Transduction of NCI-H446 CIAPIN1-negative cell, with Ad-CIAPIN1 can inhibit cell growth, suggesting that CIAPIN1 can be a new tumor-related suppressor gene.