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Neohesperidin Dihydrochalcone Alleviates Lipopolysaccharide-Induced Vascular Endothelium Dysfunction by Regulating Antioxidant Capacity.
Immun Inflamm Dis
December 2024
Department of Geriatric Intensive Medicine, Guangdong Provincial Geriatrics Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Article Synopsis
- - This study investigates the impact of neohesperidin dihydrochalone (NHDC) on endothelial dysfunction caused by sepsis, specifically how it can counteract the damaging effects of lipopolysaccharide (LPS) on blood vessels.
- - Researchers conducted various in vivo and in vitro tests to evaluate NHDC's effectiveness in alleviating vascular leakage, enhancing cell survival, and improving antioxidant responses in human umbilical vein endothelial cells (HUVECs).
- - Results showed that NHDC significantly reduced inflammation and oxidative stress by inhibiting harmful cytokines and signaling pathways, suggesting its potential as a protective treatment for vascular dysfunction related to sepsis.
Establishment of a 3D multi-layered in vitro model of inflammatory bowel disease.
J Control Release
January 2025
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal; INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal; IUCS-CESPU - Instituto Universitário de Ciências da Saúde, Rua Central de Gandra 1317, 4585-116 Gandra, Portugal. Electronic address:
Article Synopsis
- Crohn's Disease and Ulcerative Colitis are serious gastrointestinal disorders that currently have no cure, emphasizing the need for better research models to test new therapies.
- A new three-dimensional (3D) in vitro model mimics the IBD environment by incorporating multiple layers of tissue and immune responses, which includes human intestinal cells and macrophages.
- This innovative model allows for inducing inflammation similar to that seen in IBD, improving drug testing accuracy and potentially reducing reliance on animal studies while aiding in the understanding of disease mechanisms.
Toosendanin alleviates acute lung injury by reducing pulmonary vascular barrier dysfunction mediated by endoplasmic reticulum stress through mTOR.
Phytomedicine
January 2025
Department of Blood Transfusion, Key Laboratory of Jiangxi Province for Transfusion Medicine, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, PR China. Electronic address:
Background: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe clinical conditions with limited treatment options. Toosendanin (TSN), a triterpenoid compound with anti-inflammatory effects, has unclear efficacy in ALI.
Purpose: This study aimed to evaluate TSN's protective effects on ALI and the related mechanisms.
Role of Hippo/ACSL4 axis in ferroptosis-induced pericyte loss and vascular dysfunction in sepsis.
Redox Biol
December 2024
Shock and Transfusion Department, Daping Hospital, Army Medical University, Chongqing, 400042, China. Electronic address:
Sepsis is a critical condition characterized by a systemic inflammatory response to infection, often leading to severe vascular dysfunction and high mortality. One of the hallmarks of vascular dysfunction in sepsis is increased vascular permeability and the loss of pericytes, which are essential for maintaining vascular integrity. Despite the significance of pericyte loss in sepsis, the primary type of cell death responsible and the underlying molecular mechanisms remain incompletely understood.
View Article and Find Full Text PDFActivating Sig-1R inhibits microvascular permeability by reducing LRRK2 expression in lipopolysaccharide-induced acute lung injury.
Free Radic Biol Med
January 2025
Department of Anesthesiology, Anesthesiology Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China; Department of Anesthesiology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, 350212, China. Electronic address:
Background: Endothelial cells are the first and most damaged target cells during acute lung injury (ALI). Endothelial dysfunction increases pulmonary microvascular permeability, subsequently leading to pulmonary oedema and organ dysfunction; however, clinical treatments against microvascular permeability show poor efficacy. Herein, we aimed to explore the role of the Sigma-1 receptor (Sig-1R) in pulmonary microvascular permeability by constructing ALI animal and cell models, and further investigated the specific mechanisms.
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