To investigate the efficacy of sevoflurane combined with intercostal block in lung cancer surgery.

A retrospective analysis was conducted on 252 patients who underwent lung cancer surgery between January 2020 and December 2023. Patients were divided into two groups: the sevoflurane with intercostal block group (Group S, n = 108) and the propofol group (Group P, n = 144). Anesthesia protocols involved sevoflurane and intercostal nerve block or propofol. Postoperative pulmonary function, opioid consumption, stress response, and cognitive effects were compared between the two groups.

The VAS scores were significantly lower in Group S at postoperative 2 h (1.96 ± 0.52 vs 2.15 ± 0.56, P = 0.005) and 24 h (3.84 ± 0.95 vs 4.14 ± 0.98, P = 0.015), indicating superior pain management. Group S also showed better preservation of lung function, with higher FEV1 values at postoperative 2 hours (1.49 ± 0.29 L vs 1.36 ± 0.65 L, P = 0.033) and 24 hours (1.59 ± 0.39 L vs 1.45 ± 0.45 L, P = 0.012). Opioid consumption was lower in Group S at both postoperative 24 h (1307.52 ± 259.41 µg vs 1742.26 ± 253.12 µg, P < 0.001) and 48 h. Cognitive function was better preserved immediately post-surgery in Group S (26.03 ± 4.42 vs 24.14 ± 5.28, P = 0.003). However, adverse reactions like nausea were more common in Group S (9.26% vs 2.78%, P = 0.026).

Sevoflurane combined with intercostal block outperforms propofol in enhancing postoperative pulmonary function, reducing opioid reliance, and modulating stress responses in lung cancer surgery patients.

Acute lung injury (ALI), a multifactorial pathological condition, manifests through heightened inflammatory responses, compromised lung epithelial-endothelial barrier function, and oxidative stress, potentially culminating in respiratory failure and mortality. This study explores the intricate interplay between two crucial cellular mechanisms-extracellular vesicles (EVs) and autophagy-in the context of ALI pathogenesis and potential therapeutic interventions.EVs, bioactive membrane-bound structures secreted by cells, serve as versatile carriers of molecular cargo, facilitating intercellular communication and significantly influencing disease progression. Concurrently, autophagy, an essential intracellular degradation process, maintains cellular homeostasis and has emerged as a promising therapeutic target in ALI and acute respiratory distress syndrome.Our research unveils a fascinating "EV-Autophagy dual-drive pathway," characterized by reciprocal regulation between these two processes. EVs modulate autophagy activation and inhibition, while autophagy influences EV production, creating a dynamic feedback loop. This study posits that precise manipulation of this pathway could revolutionize ALI treatment strategies.By elucidating the mechanisms underlying this cellular crosstalk, we open new avenues for targeted therapies. The potential for engineered EVs to fine-tune autophagy in ALI treatment is explored, alongside innovative concepts such as EV-based vaccines for ALI prevention and management. This research not only deepens our understanding of ALI pathophysiology but also paves the way for novel, more effective therapeutic approaches in critical care medicine.

Sepsis-induced acute lung injury (ALI) is a major cause of death among patients with sepsis in intensive care units. By analyzing a model of sepsis-induced ALI using lipopolysaccharide (LPS) and cecal ligation and puncture (CLP), treatment methods and strategies to protect against ALI were discussed, which could provide an experimental basis for the clinical treatment of sepsis-induced ALI. Recent studies have found that an imbalance in autophagy, ferroptosis, and pyroptosis is a key mechanism that triggers sepsis-induced ALI, and regulating these death mechanisms can improve lung injuries caused by LPS or CLP. This article summarized and reviewed the mechanisms and regulatory networks of autophagy, ferroptosis, and pyroptosis and their important roles in the process of LPS/CLP-induced ALI in sepsis, discusses the possible targeted drugs of the above mechanisms and their effects, describes their dilemma and prospects, and provides new perspectives for the future treatment of sepsis-induced ALI.

Acute lung injury (ALI) is characterized by acute respiratory failure with tachypnea and widespread alveolar infiltrates, badly affecting patients' health. Desflurane (Des) is effective against lung injury. However, its mechanism in ALI remains unknown. BEAS-2B cells were incubated with lipopolysaccharide (LPS) to construct an ALI cell model. Cell apoptosis was evaluated using flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was employed to examine the levels of inflammatory cytokines. Interactions among let-7b-5p, homeobox A9 (HOXA9), and suppressor of cytokine signaling 2 (SOCS2) were verified using Dual luciferase activity, chromatin immunoprecipitation (ChIP), and RNA pull-down analysis. All experimental data of this study were derived from three repeated experiments. Des treatment improved LPS-induced cell viability, reduced inflammatory cytokine (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6)) levels, decreased cell apoptosis, down-regulated the pro-apoptotic proteins (Bcl-2-associated X protein (Bax) and cleaved caspase 3) expression, and up-regulated the anti-apoptotic protein B-cell-lymphoma-2 (Bcl-2) expression in LPS-induced BEAS-2B cells. Des treatment down-regulated let-7b-5p expression in LPS-induced BEAS-2B cells. Moreover, let-7b-5p inhibition improved LPS-induced cell injury. let-7b-5p overexpression weakened the protective effects of Des. Mechanically, let-7b-5p could negatively modulate HOXA9 expression. Furthermore, HOXA9 inhibited the NF-κB signaling by enhancing SOCS2 transcription. HOXA9 overexpression weakened the promotion of let-7b-5p mimics in LPS-induced cell injury. Des alleviated LPS-induced ALI via regulating let-7b-5p/ HOXA9/NF-κB axis.

LINC00839 has captured significant attention within a spectrum of human disorders, including acute lung injury, osteoarthritis, and childhood obesity. Notably, aberrant expression patterns of LINC00839 have been observed across diverse cancer tissues and cell lines. LINC00839 emerges as an oncogenic factor in tumorigenesis and exerts a positive influence on tumor-associated behaviors. Its therapeutic potential for various cancers is underscored by its modulatory impact on pivotal signaling pathways, such as PI3K/AKT, OXPHOS, and Wnt/β-catenin. Additionally, LINC00839's role in reducing sensitivity to drug and radiotherapy interventions presents opportunities for targeted intervention. Furthermore, elevated LINC00839 expression indicates advanced clinicopathological features and foretells unfavorable prognoses, as validated by publications and comprehensive analyses of tumor types using TCGA datasets. This review elucidates the multiple regulatory mechanisms and functional implications of LINC00839 in various diseases, especially malignancies, emphasizing its potential as a predictive biomarker and therapeutic target across multiple disease domains in humans.

Propofol and sevoflurane are commonly used anesthetic agents for maintenance anesthesia during radical resection of gastric cancer. However, there is a debate concerning their differential effects on cognitive function, anxiety, and depression in patients undergoing this procedure.

To compare the effects of propofol and sevoflurane anesthesia on postoperative cognitive function, anxiety, depression, and organ function in patients undergoing radical resection of gastric cancer.

A total of 80 patients were involved in this research. The subjects were divided into two groups: Propofol group and sevoflurane group. The evaluation scale for cognitive function was the Loewenstein occupational therapy cognitive assessment (LOTCA), and anxiety and depression were assessed with the aid of the self-rating anxiety scale (SAS) and self-rating depression scale (SDS). Hemodynamic indicators, oxidative stress levels, and pulmonary function were also measured.

The LOTCA score at 1 d after surgery was significantly lower in the propofol group than in the sevoflurane group. Additionally, the SAS and SDS scores of the sevoflurane group were significantly lower than those of the propofol group. The sevoflurane group showed greater stability in heart rate as well as the mean arterial pressure compared to the propofol group. Moreover, the sevoflurane group displayed better pulmonary function and less lung injury than the propofol group.

Both propofol and sevoflurane could be utilized as maintenance anesthesia during radical resection of gastric cancer. Propofol anesthesia has a minimal effect on patients' pulmonary function, consequently enhancing their postoperative recovery. Sevoflurane anesthesia causes less impairment on patients' cognitive function and mitigates negative emotions, leading to an improved postoperative mental state. Therefore, the selection of anesthetic agents should be based on the individual patient's specific circumstances.

Recently, evidence has shown that microRNA-100-3p (miR-100-3p) has been revealed as a tumor suppressor in diverse human diseases, while its capability in lung cancer warrants further validation. In this work, we aimed to discuss the impact of sevoflurane on biological functions of lung cancer cells by modulating the miR-100-3p/sterol O-acyltransferase 1 (SOAT1) axis. Lung cancer cell lines (A549 and H460) were treated with various concentrations of sevoflurane. Cell viability, proliferation, migration, and invasion were evaluated using MTT, colony formation, wound healing, and transwell assays. Moreover, miR-100-3p and SOAT1 expressions were evaluated by reverse transcription-quantitative polymerase chain reaction in lung cancer cells. The target interaction between miR-100-3p and SOAT1 was predicted by bioinformatics analysis and verified by the dual-luciferase reporter gene assay. The findings of our work demonstrated that sevoflurane impeded the abilities on viability, proliferation, migration, and invasion of A549 and H460 cells. The expression of miR-100-3p was reduced, and SOAT1 expression was elevated in lung cancer cells. miR-100-3p targeted SOAT1. Besides, sevoflurane could lead to expressed improvement of miR-100-3p or limitation of SOAT1. Downregulation of miR-100-3p or upregulation of SOAT1 restored the suppression of sevoflurane on abilities of viability, proliferation, migration, and invasion in A549 and H460 cells. In the rescue experiment, downregulation of SOAT1 reversed the impacts of downregulation of miR-100-3p on sevoflurane on lung cancer cells. Collectively, our study provides evidence that sevoflurane restrained the proliferation and invasion in lung cancer cells by modulating the miR-100-3p/SOAT1 axis. This article provides a new idea for further study of the pathogenesis of lung cancer.

Bone marrow mesenchymal stem cell (BMSC)-derived exosomes can protect lung tissues against sepsis, but its related mechanism remains elusive. BMSCs were primed with or without lipopolysaccharide (LPS) before extracting exosomes. The isolated exosomes were identified by transmission electron microscopy, nanoparticle tracking analysis, and western blot. LPS-stimulated macrophages were cocultured with exosomes for 24 h, followed by enzyme-linked immunosorbent assay, flow cytometry, and molecular experiments. Bioinformatics and luciferase assay were employed to investigate the interaction between miR-150-3p and inhibin subunit beta A (INHBA). MiR-150-3p expression was increased in exosomes in a proinflammatory environment. Exosomes suppressed proinflammatory polarization by downregulating IL-6, IL-1β, iNOS, and CD86, as well as promoted anti-inflammatory polarization by upregulating IL-10, ARG-1, and CD206 in LPS-stimulated macrophages. Such effects were more pronounced by LPS-primed exosomes, which was reversed in the absence of miR-150-3p. MiR-150-3p targeted INHBA. INHBA silencing decreased CD86 expression and increased CD206 expression in macrophages, but these effects were reversed by exosomal miR-150-3p inhibition. Proinflammatory BMSC-derived exosomal miR-150-3p suppressed proinflammatory polarization and promoted anti-inflammatory polarization of alveolar macrophages to attenuate LPS-induced sepsis by targeting INHBA.

Small noncoding RNAs, known as microRNAs (miRNAs), are vital for the regulation of diverse biological processes. miR-223, an evolutionarily conserved anti-inflammatory miRNA expressed in cells of the myeloid lineage, has been implicated in the regulation of monocyte-macrophage differentiation, proinflammatory responses, and the recruitment of neutrophils. The biological functions of this gene are regulated by its expression levels in cells or tissues. In this review, we first outline the regulatory role of miR-223 in granulocytes, macrophages, endothelial cells, epithelial cells and dendritic cells (DCs). Then, we summarize the possible role of miR-223 in chronic obstructive pulmonary disease (COPD), acute lung injury (ALI), coronavirus disease 2019 (COVID-19) and other pulmonary inflammatory diseases to better understand the molecular regulatory networks in pulmonary inflammatory diseases.