Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Galectin-3 is a β-galactoside-binding lectin implicated as a mediator in a variety of inflammatory and fibrotic diseases. However, information about galectin-3 release in patients with acute respiratory distress syndrome (ARDS) is very limited. We sought to determine whether plasma galectin-3 levels were increased in ARDS patients and were associated with disease severity. ⋯ Higher levels of galectin-3 were significantly associated with disease severity and worse outcomes in ARDS patients.
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Simvastatin has lung vascular-protective effects via augmentation of endothelial barrier function. Accordingly, on the basis of our previous study, we hypothesized that endothelial cell (EC) protection by simvastatin is dependent on the stabilization on cytoskeletons. ⋯ An increased serous EMP level associated with Cdc42-PAK4 can be deemed as a useful pulmonary injury marker in LPS-treated mice, and our results might be more relevant in guiding the clinical treatment of ALI by intervening Cdc42-PAK4 or EMPs.
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Hepatoprotective Effects of Corilagin Following Hemorrhagic Shock are Through Akt-Dependent Pathway.
Corilagin, a component of Phyllanthus urinaria extract, possesses antioxidant, thrombolytic, antiatherogenic, and hepatoprotective properties, but the mechanism underlying these effects remains unclear. Previous studies showed that the Akt (protein kinase B) signaling pathway exerts anti-inflammatory and organ protective effects. The aim of this study was to investigate the mechanism of action of corilagin and determine whether these effects are mediated through the Akt-dependent pathway in a trauma-hemorrhagic shock-induced liver injury rodent model. ⋯ Hepatic phospho-Akt expression was also higher in corilagin-treated rats than in vehicle-treated rats. The elevation of phospho-Akt was abolished by combined treatment with Wortmannin and corilagin. Our results suggest that corilagin exerts its protective effects on hemorrhagic shock-induced liver injury, at least, via the Akt-dependent pathway.
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New definitions of sepsis and septic shock were published in early 2016, updating old definitions that have not been revisited since 2001. These new definitions should profoundly affect sepsis research. ⋯ In contrast to previous approaches, these new clinical criteria are evidence based. In this review, two of the authors of the new definitions detail the content of the papers and explore the implications for shock and sepsis researchers.
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Sepsis is the leading cause of death among critically ill patients and natural killer T (NKT) cell activation is essential to induce inflammatory cytokine cascade in sepsis. However, little is known about what regulates the NKT cell function during sepsis. Herein, we showed that T-cell immunoglobulin and mucin domain 3 (Tim-3) expression in NKT cells is elevated in experimental mice during sepsis. ⋯ Administration of α-lactose to block Tim-3 signaling pathway significantly improved the survival of septic mice, concomitant with reduced IL-12 production by dendritic cells, reduced Tim-3 expression, prevented NKT cell apoptosis, and attenuated production of inflammatory cytokines. Collectively, Tim-3 signaling in NKT cells plays a critical role in the immunopathogenesis of sepsis. Thus, α-lactose could be a promising immunomodulatory agent in the treatment of sepsis.