Exogenous cytochrome c inhibits the expression of transforming growth factor-β1 in a mouse model of sepsis-induced myocardial dysfunction via the SMAD1/5/8 signaling pathway
The current study investigated the role of exogenous cytochrome c in sepsis-induced myocardial dysfunction (SIMD) using a mouse model and aimed to elucidate its effect on transforming growth factorβ1 (TGFβ1) expression during this process. A total of 75 male Kunming mice were randomly divided into the following five group: Normal (N, n=15); shamoperation (SHAM, n=15); sepsis (CLP, n=15); normal saline (NS, n=15); and cytochrome c (Cytc, n=15). Animals were sacrificed at 0, 6 or 12 h and the samples were analyzed using transmission electron microscopy, histopathological examination, reverse transcriptionquantitative polymerase chain reaction, ELISA, protein analysis by western blotting. The SIMD model was developed and a significant downregulation of TGFβ1 gene expression, in addition to a reduction in the plasma and protein levels of TGFβ1 as well as the protein levels of TGFβ1activated SMAD 1/5/8 were observed in the CLP group. The data from the current study indicate that using exogenous cytochrome c as a therapeutic strategy for SIMD is feasible, and may function via the downregulation of TGF-β1 expression through the SMAD 1/5/8 signaling pathway.
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Document Type: Research Article
Affiliations: Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China
Publication date: August 1, 2015
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