Articles: sepsis.
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The study aimed to evaluate, for the first time, the diagnostic value of long non-coding RNA (lncRNA) small nucleolar RNA host gene 8 (SNHG8) in sepsis and its molecular mechanisms in sepsis-induced inflammation and cardiac dysfunction. ⋯ Reduced SNHG8 is a potential diagnostic biomarker for sepsis. It is involved in sepsis-induced inflammatory response and cardiac dysfunction through sponging miR-34b-5p.
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Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), induced by sepsis, is predominantly caused by inflammation injury. However, there is no clear consensus on how to regulate the inflammatory response. The TNF pathway is one of the primary inflammatory pathways activated in sepsis. cIAP1/2, an essential E3 ubiquitin ligase in the TNF pathway, plays a pivotal role in positively regulating the activation of nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways to promote inflammation while inhibiting apoptosis. ⋯ Our study shows that cIAP1/2 expression increased in the lung tissue of a CLP rat ALI model. Inhibiting cIAP1/2 with AZD5582, a second mitochondria-derived activator of caspases (SMAC) mimetic, induced increased apoptosis and reduced lung injury. Therefore, inhibiting cIAP1/2 can alleviate sepsis-induced ALI, providing a new target for regulating organ damage induced by sepsis-induced inflammatory responses.
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The purpose of the present study was to evaluate the potential relationship of lymphocyte-to-monocyte ratio (LMR) with outcomes of septic patients at intensive care unit (ICU) admission. ⋯ We report for the first time that a lower LMRmax value is independently predictive of a poor prognosis in septic patients. Therefore, as an inexpensive and readily available indicator, LMRmax may facilitate stratification of prognosis in septic patients.
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Background: Sepsis is a lethal disease due to uncontrolled inflammatory responses. Macrophages play an important role in sepsis-associated inflammation. Jing Si Herbal Tea (JSHT) is a plant-based regimen with anti-inflammatory properties designed to treat respiratory diseases; however, its underlying therapeutic mechanism remains unclear. ⋯ RAW264.7 cells exhibited filopodia protruding from the cell surface in the LPS group, which were inhibited in the Pre-JSHT and Post-JSHT groups. Conclusions: LPS induced M1 polarization with elevated inflammatory signaling and cytokine levels, while JSHT not only decreased M1 polarization but also promoted M2 polarization with decreased inflammatory responses. We propose JSHT as a potential anti-inflammatory agent against LPS-induced inflammation.
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Sepsis induces profound disruptions in cellular homeostasis, particularly impacting mitochondrial function in cardiovascular and cerebrovascular systems. This study elucidates the regulatory role of the Pyruvate Kinase M2 (PKM2)- Prohibitin 2 (PHB2) axis in mitochondrial quality control during septic challenges and its protective effects against myocardial and cerebral injuries. Employing LPS-induced mouse models, we demonstrate a significant downregulation of PKM2 and PHB2 in both heart and brain tissues post-sepsis, with corresponding impairments in mitochondrial dynamics, including fission, fusion, and mitophagy. ⋯ These cellular mechanisms translate into substantial in vivo benefits, with transgenic mice overexpressing PKM2 or PHB2 displaying remarkable resistance to sepsis-induced cardiomyocyte and neuronal apoptosis, and organ dysfunction. Our findings highlight the PKM2-PHB2 interaction as a novel therapeutic target for sepsis, providing a foundation for future research into mitochondrial-based interventions to treat this condition. The study's insights into the molecular underpinnings of sepsis-induced organ failure pave the way for potential clinical applications in the management of sepsis and related pathologies.