Tocilizumab alleviated lipopolysaccharide-induced acute lung injury by improving PI3K/AKT pathway.

Acute lung injury (ALI) is a severe inflammatory condition of the respiratory system, associated with high morbidity and mortality. This study investigates the therapeutic potential of tocilizumab (TZ), an IL-6 receptor inhibitor, in mitigating lipopolysaccharide (LPS)-induced ALI by modulating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway. An ALI model was established using LPS induction.

Autophagy in Acute Lung Injury.

Acute lung injury (ALI) is a critical condition marked by rapid-onset respiratory failure due to extensive inflammation and increased pulmonary vascular permeability, often progressing to acute respiratory distress syndrome (ARDS) with high mortality. Autophagy, a cellular degradation process essential for removing damaged organelles and proteins, plays a crucial role in regulating lung injury and repair. This review examines the protective role of autophagy in maintaining cellular function and reducing inflammation and oxidative stress in ALI.

Review on the Role of Mitochondrial Dysfunction in Septic Encephalopathy.

Septic Encephalopathy (SE) is a frequent and severe complication of sepsis, characterized by a range of neurocognitive impairments from mild confusion to deep coma. The underlying pathophysiology of SE involves systemic inflammation, neuroinflammation, blood-brain barrier (BBB) disruption, and mitochondrial dysfunction. Among these factors, mitochondrial dysfunction plays a pivotal role, contributing to impaired ATP production, increased reactive oxygen species (ROS) generation, and activation of apoptotic pathways, all of which exacerbate neuronal damage and cognitive deficits.

Fortunellin ameliorates LPS-induced acute lung injury, inflammation, and collagen deposition by restraining the TLR4/NF-κB/NLRP3 pathway.

Objective: Acute lung injury (ALI) is the prevalent respiratory disease of acute inflammation with high morbidity and mortality. Fortunellin has anti-inflammation property, but its role in ALI remains elusive. Thus, this study clarified the function of fortunellin on ALI pathogenesis.

Songorine ameliorates LPS-induced sepsis cardiomyopathy by Wnt/β-catenin signaling pathway-mediated mitochondrial biosynthesis.

Septic cardiomyopathy (SCM) is manifested by impairment of cardiac contractile function with myocardial mitochondrial dysregulation. Natural product, songorine (SGR), a diterpenoid alkaloid derived from the lateral root of Aconitum carmichaeli, has been reported for the treatment of heart failure. Here, the protective role of SGR in heart injury of SCM was investigated and its underlying action of mechanism was explored.

Sivelestat sodium alleviated lipopolysaccharide-induced acute lung injury by improving endoplasmic reticulum stress.

Acute lung injury (ALI) is a common inflammatory respiratory disorder characterized by a high incidence and mortality rate. This study aimed to investigate the potential therapeutic effects of the neutrophil elastase inhibitor Sivelestat sodium (SIV) in improving endoplasmic reticulum stress (ERS) while treating lipopolysaccharide (LPS)-induced ALI. An ALI model was established using LPS induction.

Penehyclidine hydrochloride protects against lipopolysaccharide-induced acute lung injury by promoting the PI3K/Akt pathway.

Introduction: Acute lung injury (ALI) attracted attention among physicians because of its high mortality. We aimed to determine whether the phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt) pathway is involved in the protective effects of penehyclidine hydrochloride (PHC) against lipopolysaccharide (LPS)-induced ALI.

Methods: H&E staining was used to observed pathological changes in the lung tissues.

Konjac glucomannan defends against high-fat diet-induced atherosclerosis in rabbits by promoting the PI3K/Akt pathway.

Atherosclerosis (AS) is the main cause of cardiovascular disease and cerebral infarction, which seriously endanger human health. This study aimed to investigate konjac glucomannan (KGM) defends against high-fat diet-induced AS in rabbits by promoting the PI3K/Akt pathway. KGM administration reduced the degree of AS indicated by reducing the plaques and foam cells, the tunica intima thickness, and the tunica intima/tunica media thickness ratio in the aorta, and enlarging the lumen of the aorta.

Therapeutic Plasma Exchange Protects Patients with Sepsis-Associated Disseminated Intravascular Coagulation by Improving Endothelial Function.

The mortality rate of sepsis-associated disseminated intravascular coagulation (DIC) is high. This study aimed to explore the efficacy of therapeutic plasma exchange (TPE) in sepsis-associated DIC patients by improving endothelial function. A total of 112 sepsis-associated DIC patients were randomly divided into the TPE group (n = 40), the heparin (HP) group (n = 36), and the SHAM group (n = 36).

Transcriptomic study of lipopolysaccharide-induced sepsis damage in a mouse heart model.

Sepsis is an emergency systemic illness caused by pathogen infection and the combined result of the underactivity and overactivity of a patient's own immune system. However, the molecular mechanism of this illness remains largely unknown. Lipopolysaccharide (LPS) was injected to establish a sepsis model, and heart tissue was used to analyze transcriptome changes in mice.

Penehyclidine hydrochloride defends against LPS-induced ALI in rats by mitigating endoplasmic reticulum stress and promoting the Hes1/Notch1 pathway.

Penehyclidine hydrochloride (PHC) is a novel anticholinergic drug applied broadly in surgeries as a preanesthetic medication. A substantial amount of research indicates that PHC has lung defensive properties. Considering that endoplasmic reticulum (ER) stress exerts a crucial function in cell apoptosis associated with the lipopolysaccharides (LPS)-induced acute lung injury (ALI) model, we aimed to determine whether regulation of ER stress in the LPS-induced ALI model was associated with the lung defensive role of PHC.