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Selenium, reported as an important medium for maintaining the body's homeostasis, acts to have multiple bioeffects including anti-inflammatory, anti-oxidant and anti-apoptosis effects. However, its role in heart failure still remains unclear. In this study, we explored the effects of selenium on heart failure and its possible mechanism. The heart failure models were induced by aortic banding and isoproterenol. H&E, TUNEL and PSR staining were performed to detect the degree of cardiomyocyte hypertrophy, apoptosis rates and heart fibrosis, respectively. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect different mRNA levels, and western blot was applied to assess the expressions of relative proteins. Immunofluorescence staining was used to evaluate α-SMA density. We first found that treatment of selenium alleviated heart fibrosis and the development of heart failure but not cardiomyocyte cross sectional areas. Besides, selenium improved heart levels of superoxide dismutase2 (SOD2), glutathione peroxidase (Gpx) and glutathione (GSH) and the activity of SOD, accompanied by decreased apoptosis rate. In addition, our in vitro study has shown that selenium reduced mRNA levels of collagen Ⅰ and collagen III, expressions of a-SMA, p-AKT/AKT and p-GSK-3β/ GSK-3β, apoptosis rates and reactive oxygen species (ROS) levels in H9C2 cardio-myoblasts treated with TGF-β1. Moreover, the level of Sirt1 was found to be up-regulated by selenium which effects were weakened after the administration of small interfering RNA (siRNA)-Sirt1 or EX527 (inhibitor of Sirt1). Our current results have demonstrated that the protective effects of selenium on heart hypertrophy is through the regulation of Sirt1 and AKT/GSK-3β pathway., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

The lipopolysaccharide (LPS)-Toll-like receptor 4 (TLR4) signaling pathway in alveolar epithelial cells plays an important role in many pathologic processes such as acute lung injury (ALI). The single immunoglobulin IL-1 receptor-related protein (SIGIRR) is an inhibitor of LPS-TLR4 signaling, but its expression and function in alveolar epithelial cells are still unknown. In this study, we examined the expression of SIGIRR in normal human lung tissue using immunohistochemistry, reverse transcription-PCR (RT-PCR) and Western blot and found that SIGIRR was expressed in alveolar epithelial cells. Treatment of an alveolar epithelial cell line, A549, with LPS and we observed a downregulation of SIGIRR mRNA, which returned to normal levels 24h after LPS exposure. A549 cells were then transfected with a SIGIRR eukaryotic expression vector to over-express SIGIRR or, as a control, with an empty vector. Following LPS exposure, the transcriptional activity of NF-kappaB was measured using a dual-luciferase reporter assay system, and the concentration of IL-1beta, TNF-alpha and IL-6 was determined by ELISA, and cell proliferation was measured by MTT. In A549 cells that over-expressed SIGIRR, LPS treatment resulted in a significant decrease in the transcriptional activity of NF-kappaB and cell growth inhibition ratio, as well as lower levels of secreted IL-1beta, TNF-alpha and IL-6. In conclusion, SIGIRR in A549 cells inhibits the transcriptional activity of NF-kappaB and reduces the amount cytokines produced, protecting these cells from acute LPS-induced damage., (Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.)