华西虚拟期刊

华西虚拟期刊

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Ischemia-induced stroke is the most common disease of the nervous system and is associated with a high mortality rate worldwide. Cerebral ischemia may lead to remote organ dysfunction, particular in the lungs, resulting in lung injury. Nowadays, bone marrow-derived mesenchymal stem cells (BMSCs) are widely studied in clinical trials as they may provide an effective solution to the treatment of neurological and cardiac diseases; however, the underlying molecular mechanisms remain unknown. In this study, a model of permanent focal cerebral ischemia-induced lung injury was successfully established and confirmed by neurological evaluation and lung injury scores. We demonstrated that the transplantation of BMSCs (passage 3) via the tail vein into the lung tissues attenuated lung injury. In order to elucidate the underlying molecular mechanisms, we analyzed the gene expression profiles in lung tissues from the rats with focal cerebral ischemia and transplanted with BMSCs using a Gene microarray. Moreover, the Gene Ontology database was employed to determine gene function. We found that the phosphoinositide 3-kinase (PI3K)-AKT signaling pathway, transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF) were downregulated in the BMSC transplantation groups, compared with the control group. These results suggested that BMSC transplantation may attenuate lung injury following focal cerebral ischemia and that this effect is associated with the downregulation of TGF-beta, PDGF and the PI3K-AKT pathway.

Key words: ACUTE KIDNEY INJURY; STROMAL CELLS; PULMONARY-FIBROSIS; GROWTH-FACTOR; BIOINFORMATICS ANALYSIS; REPERFUSION INJURY; BRAIN; DYSFUNCTION; APOPTOSIS; STROKE

引用本文: . . 华西虚拟期刊, 2000, 1(1): 57-70-. doi: 10.3892/ijmm.2016.2819 复制

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