Post‑operative cognitive dysfunction (POCD) is a severe complication characterized by cognitive decline in patients following anesthesia and surgery. Previous studies have suggested that volatile anesthetics, for example isoflurane, may contribute to such impairment. In the present study, the effects of emulsified isoflurane (EI) exposure on cognitive function, as well as the potential mechanisms, were investigated in animal models. Eight‑month‑old male rats were administered a single intravenous injection of 8% EI. The rats were then subjected to the Morris water maze test to assess their cognitive functions at different time‑points following drug administration. Samples were taken in order to detect the plasma corticosterone concentration and the levels of hippocampal brain‑derived neurotrophic factor (BDNF) and nerve growth factor (NGF), as well as the expression of BDNF and NGF in the hippocampal region. The results showed that a single injection of EI caused reversible learning and memory dysfunction in adult rats. It was found that downregulation of BDNF expression may contribute to the isoflurane‑induced cognitive impairment of these rats. Increased expression of NGF may be associated with the protection mechanism subsequent to learning and memory function decline, and therefore may accelerate the recovery of cognitive function.

Emergence delirium (ED) is delirium that occurs during or immediately after emergence from general anesthesia or sedation. Effective pharmacological treatments for ED are lacking, so preventive measures should be taken to minimize the risk of ED. However, the risk factors for ED in adults are unclear. In this systematic review and meta-analysis, we evaluated the evidence for risk factors for ED in adults. The PubMed, Scopus, Cochrane Library, Google Scholar, and Embase databases were searched for observational studies reporting the risk factors for ED in adults from inception to July 31, 2023. Twenty observational studies reporting 19,171 participants were included in this meta-analysis. Among the preoperative factors identified as risk factors for ED were age <40 or ≥65 years, male sex, smoking history, substance abuse, cognitive impairment, anxiety, and American Society of Anesthesiologists physical status score III or IV. Intraoperative risk factors for ED were the use of benzodiazepines, inhalational anesthetics, or etomidate, and surgical factors including abdominal surgery, frontal craniotomy (vs. other craniotomy approaches) for cerebral tumors, and the length of surgery. Postoperative risk factors were indwelling urinary catheters, the presence of a tracheal tube in the postanesthetic care unit or intensive care unit, the presence of a nasogastric tube, and pain. Knowledge of these risk factors may guide the implementation of stratified management and timely interventions for patients at high risk of ED. The majority of studies included in this review investigated only hyperactive ED and further research is required to determine risk factors for hypoactive and mixed ED types.

Neurodegenerative diseases (NDs), such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and motor neuron disease, are diseases characterized by neuronal damage and dysfunction. NDs are considered to be a multifactorial disease with diverse etiologies (immune, inflammatory, aging, genetic, etc.) and complex pathophysiological processes. Previous studies have found that neuroinflammation and typical microglial activation are important mechanisms of NDs, leading to neurological dysfunction and disease progression. Pyroptosis is a new mode involved in this process. As a form of programmed cell death, pyroptosis is characterized by the expansion of cells until the cell membrane bursts, resulting in the release of cell contents that activates a strong inflammatory response that promotes NDs by accelerating neuronal dysfunction and abnormal microglial activation. In this case, abnormally activated microglia release various pro-inflammatory factors, leading to the occurrence of neuroinflammation and exacerbating both microglial and neuronal pyroptosis, thus forming a vicious cycle. The recognition of the association between pyroptosis and microglia activation, as well as neuroinflammation, is of significant importance in understanding the pathogenesis of NDs and providing new targets and strategies for their prevention and treatment.

General anesthesia, as a commonly used medical intervention, has been widely applied during surgical procedures to ensure rapid loss of consciousness and pain relief for patients. However, recent research suggests that general anesthesia may be associated with the occurrence of perioperative neurocognitive disorder (PND). PND is characterized by a decline in cognitive function after surgery, including impairments in attention, memory, learning, and executive functions. With the increasing trend of population aging, the burden of PND on patients and society’s health and economy is becoming more evident. Currently, the clinical consensus tends to believe that peripheral inflammation is involved in the pathogenesis of PND, providing strong support for further investigating the mechanisms and prevention of PND.

Aim. To investigate the protective effects of budesonide against lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in a murine model and its underlying mechanism.Methods. Adult male C57BL/6 mice were divided into three groups: control, ALI, and ALI + budesonide groups. LPS (5 mg/kg) was intratracheally injected to induce ALI in mice. Budesonide (0.5 mg/kg) was intranasally given 1 h before LPS administration in the ALI + budesonide group. Twelve hours after LPS administration, all mice were sacrificed. Hematoxylin-eosin staining and pathological scores were used to evaluate pathological injury. Bronchoalveolar lavage was performed. The numbers of total cells, neutrophils, and macrophages in the bronchoalveolar lavage fluid (BALF) were counted. Enzyme-linked immunosorbent assay was employed to detect the proinflammatory cytokines in BALF and serum, including tumor necrosis factor- (TNF-)α, monocyte chemoattractant protein- (MCP-) 1, and interleukin- (IL-) 1β. The expression of the nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome was detected by western blotting. A lethal dose of LPS (40 mg/kg, intraperitoneally) was injected to evaluate the effects of budesonide on survival rates.Results. Budesonide pretreatment dramatically attenuated pathological injury and reduced pathological scores in mice with ALI. Budesonide pretreatment obviously reduced the numbers of total cells, neutrophils, and macrophages in the BALF of mice with ALI. Additionally, budesonide dramatically reduced TNF-αand MCP-1 expression in the BALF and serum of mice with ALI. Budesonide significantly suppressed NLRP3 and pro-caspase-1 expression in the lung and reduced IL-1βcontent in the BALF, indicating that budesonide inhibited the activation of the NLRP3 inflammasome. Furthermore, we found that budesonide improved the survival rates of mice with ALI receiving a lethal dose of LPS.Conclusion. Suppression of NLRP3 inflammasome activation in mice via budesonide attenuated lung injury induced by LPS in mice with ALI.