Infections caused byCandida albicans, often refractory and with high morbidity and mortality, cause a heavy burden on the public health while the current antifungal drugs are limited and are associated with toxicity and resistance. Many plant-derived molecules including compounds isolated from traditional Chinese medicine (TCM) are reported to have antifungal activity through different targets such as cell membrane, cell wall, mitochondria, and virulence factors. Here, we review the recent progress in the anti-Candidacompounds from TCM, as well as their antifungal mechanisms. Considering the diverse targets and structures, compounds from TCM might be a potential library for antifungal drug development.

Sepsis-associated encephalopathy (SAE) is a frequent brain dysfunction found in sepsis patients, manifesting as delirium, cognitive impairment, and abnormal behaviors. The gut microbiome and short-chain fatty acids (SCFAs) are particularly associated with neuroinflammation in patients with SAE, thus noticeably attracting scholars’ attention. The association of brain function with the gut-microbiota-brain axis was frequently reported. Although the occurrence, development, and therapeutic strategies of SAE have been extensively studied, SAE remains a critical factor in determining the long-term prognosis of sepsis and is typically associated with high mortality. This review concentrated on the interaction of SCFAs with microglia in the central nervous system and discussed the anti-inflammatory and immunomodulatory effects of SCFAs by binding to free fatty acid receptors or acting as histone deacetylase inhibitors. Finally, the prospects of dietary intervention using SCFAs as dietary nutrients in improving the prognosis of SAE were reviewed.

Purpose: Maresin 1 (MaR1) is a specialized pro-resolving mediator with anti-inflammatory properties that promotes tissue repair. This study aims to investigate the molecular involvement of MaR1 in protecting against sepsis-induced acute liver injury (SI-ALI). Methods: In vivo, a murine SI-ALI model was established using the cecal ligation and puncture (CLP) paradigm, providing a system in which the mechanistic functions of MaR1 could be tested. These analyses were supplemented through in vitro assays in which Alpha mouse liver 12 (AML12) hepatocytes and RAW264.7 macrophages were co-cultured in a Transwell system, with lipopolysaccharide (LPS) stimulation being used to establish a sepsis model. These cells were treated with MaR1 and/or nuclear factor erythroid 2-related factor 2 (Nrf2)inhibitor, while lentiviral transduction was used to knock down Nrf2 within AML12 cells. Hepatic pathological damage was assessed through hematoxylin and eosin staining. Lipid peroxidation-related analyses were conducted through the use of thiobarbituric acid, ferrous ions, glutathione, and appropriate fluorescent probes for reactive oxygen species detection. Liver enzymes and inflammatory mediators were quantified using appropriate Enzyme-Linked Immunosorbent Assays (ELISAs). Protein concentrations were evaluated via Western blot analysis. Results: The presence of ferroptosis in SI-ALI. MaR1 was found to proficiently suppress ferroptosis in SI-ALI. Mechanistically, MaR1 enhanced Nrf2 expression in AML12 hepatocytes, while the Nrf2 inhibitor ML-385 or Nrf2 siRNA mitigated MaR1’s regulatory influence on ferroptosis. Meanwhile, the expressions of the downstream genes solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) diminished, suggesting that MaR1 has a protective function via activating the Nrf2/SLC7A11/GPX4 pathway to mitigate ferroptosis in septic liver injury. Conclusion: The results indicate that MaR1 mitigates SI-ALI via stimulating the Nrf2/SLC7A11/GPX4 pathway to suppress ferroptosis. Moreover, it offers significant potential as a new agent for the prevention of SI-ALI.

Glucagon-like peptide-1 (GLP-1) has been widely studied in the context of treating obesity and various forms of metabolic disease. Sepsis is a life-threatening medical emergency characterized by the widespread dysregulation of energy metabolism within cells. The potential for GLP-1 to improve sepsis patient outcomes through improvements in energy metabolism and inflammation has been a focus of growing research interest, with many studies of GLP-1 itself and related compounds, including GLP-1 receptor agonists (GLP-1RAs), and dipeptidyl peptidase-4 (DPP-4) inhibitors, having explored the impact on sepsis in cells and organs. Such studies require that attention be paid to both the physiological and potential pathological effects of GLP-1 in sepsis. In many reports, researchers have demonstrated that endogenous GLP-1, GLP-1RAs, or DPP-4 inhibitors (a GLP-1 depressant) can modulate glucose homeostasis, inflammatory activity, immune function, and organ dysfunction in studies of sepsis model systems in vitro and in vivo. To date, GLP-1-based treatments have yet to be specifically used to manage sepsis, but its pleiotropic effects suggest its significant potential in sepsis treatment. This review provides an overview of the relationship between GLP-1 and its related compounds with sepsis, aiming to offer novel perspectives for the diagnosis and treatment of this condition. It highlights that GLP-1 may serve as a new biomarker for assessing the severity and prognosis of sepsis, and potentially contribute to improving clinical outcomes in septic patients. Meanwhile, GLP-1 may function as a messenger of metabolic reprogramming, shifting cellular energy production from oxidative phosphorylation to glycolysis, thereby modulating immune responses and influencing inflammatory reactions to enhance the clearance of pathogens. However, GLP-1 may act as a double-edged sword, the enhanced inflammatory response can potentially induce cytotoxic and organ-damaging effects while exerting beneficial actions.

Sepsis, a life-threatening condition characterized by organ dysfunction resulting from severe infection, has gained considerable attention for the involvement of mitochondrial (mt) dysfunction in disrupting cellular energy metabolism and exacerbating inflammatory injury through the release of mt components. During sepsis, damage to the mt electron transport chain (ETC) in various organs impairs the mitochondria's ability to sustain ATP production and effectively use oxygen. This dysfunction also increases mt membrane permeability, releasing mt damage-associated molecular patterns (DAMPs), i.e., proteins, phospholipids, metabolites, nucleic acids (NA), and reactive oxygen species (ROS). These DAMPs synergize with pathogen-associated molecular patterns (PAMPs) to amplify systemic inflammation and organ injury. Despite advances in understanding mt-driven metabolic and immune dysregulation, translating these insights into effective therapeutic interventions remains challenging. This review explores the dual role of mitochondria in sepsis, functioning both as central regulators of cellular metabolism and as key modulators of inflammatory responses. It evaluates mt-targeted therapeutic strategies, including metabolic reprogramming, induction of mt biogenesis, antioxidant approaches, and stabilization of mt membranes. Integrating findings from both preclinical and clinical studies highlights potential therapeutic avenues to alleviate sepsis-induced organ dysfunction and improve patient outcomes.