Signa Vitae最新文献

{"title":"Clematichinenoside AR improves isoflurane-stimulated cognitive dysfunction in aged mice by ameliorating neurotoxicity through ERK-CREB pathway","authors":"Jingjing Hu, Yuanfang Li, Guoqiang Fei","doi":"10.22514/sv.2025.059","DOIUrl":"https://doi.org/10.22514/sv.2025.059","url":null,"abstract":"Background: Postoperative cognitive dysfunction (POCD) can result in decreased memory and information processing speed after anesthesia. Clematichinenoside AR (AR) has recently been recognized for its multiple biological activities, including anti-inflammatory and anti-apoptotic properties. However, its effectiveness in alleviating symptoms of POCD is not yet well understood. Our objective is to evaluate and explore the role of AR in addressing POCD. Methods: Mice were divided into 5 groups: sham, isoflurane, isoflurane + AR (8 mg/kg), isoflurane + AR (16 mg/kg) and isoflurane + AR (32 mg/kg). The Morris Water Maze (MWM) test and Fear Conditioning Test (FCT) were conducted to evaluate the role of AR in mice with POCD. Subsequently, Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and Immunoblotting were performed to confirm the effects of AR on cell apoptosis. Furthermore, Quantitative Polymerase Chain Reaction (qPCR) and Enzyme-Linked Immunosorbent Assay (ELISA) were utilized to verify the impact of AR on inflammation. The morphology of hippocampal neurons and protein expression were examined through Hematoxylin and Eosin (H&E) staining and western blot. Results: The results indicated that AR can enhance isoflurane-stimulated cognitive dysfunction in mice. In addition, AR exhibits anti-apoptotic and anti-inflammatory effects in POCD mice, highlighting its neuroprotective effects. Additionally, AR activates the Extracellular Signal-Regulated Kinase—cAMP Response Element-Binding Protein (ERK-CREB) signaling pathway. Conclusions: AR improves isoflurane-stimulated cognitive dysfunction in aged mice by ameliorating neurotoxicity.","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147918190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dendrobine promotes cardiomyocyte proliferation and inhibits apoptosis and inflammation in an in vitro acute myocardial infarction model","authors":"","doi":"10.22514/sv.2025.069","DOIUrl":"https://doi.org/10.22514/sv.2025.069","url":null,"abstract":"Background: Acute myocardial infarction (AMI) is a serious condition caused by the sudden blockage of a coronary artery, leading to heart tissue damage. The increasing number of AMI cases, particularly in younger individuals as a result of unhealthy lifestyles, highlights the demand for innovative treatments. Dendrobine, a compound from Dendrobium, has multiple biological activities, such as suppressing oxidative stress, inflammation and cell death. Methods: An in vitro AMI model was established using H9C2 rat cardiomyocytes subjected to hypoxia/reoxygenation (H/R) conditions. The effects of dendrobine on cardiomyocyte proliferation were assessed using Cell Counting Kit (CCK)8 assays and EdU staining. Apoptosis was evaluated by flow cytometry and Western blot. Inflammatory responses were measured through Enzyme-Linked Immunosorbent Assay (ELISA) and Immunoblot, and the involvement of the Nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway was examined using Western blot. Results: Dendrobine significantly promoted cardiomyocyte proliferation under H/R conditions, inhibited apoptosis in H9C2 cells, and effectively suppressed the inflammatory response. Additionally, dendrobine enhanced the activation of the Nrf2/Keap1 signaling pathway. Conclusions: Dendrobine exerts significant cardioprotective effects in an in vitro AMI model by promoting cell proliferation, suppressing programmed cell death and inflammation and regulating the Nrf2/Keap1 pathway. Therefore, dendrobine holds potential as a therapeutic agent for AMI intervention.","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"21 5","pages":"79-79"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolomics analysis and cytokine profiling in ARDS: rationale and methodology of standardized laboratory procedures for biological sample analysis","authors":"Paternoster G., Carmosino M., Milella L., Milano S., Ponticelli M., Sannicandro M., Izzi M. C., Carlucci V., Belletti A., Mongardini E., Monti G., Giardina G., Palumbo D., Ronca E., Ferrara B., Chiodi B., Oliva F. M., De Piccoli N., Di Tomasso N.","doi":"10.22514/sv.2025.141","DOIUrl":"https://doi.org/10.22514/sv.2025.141","url":null,"abstract":"Background: Acute respiratory distress syndrome (ARDS) is a life-threatening condition associated with high short-and long-term morbidity and mortality. One major limitation in the management of ARDS is its biological and clinical heterogeneity, which may explain the lack of consistent benefit observed for most therapeutic interventions in unselected patient populations. Recent studies have suggested the existence of distinct ARDS subphenotypes, potentially characterized by unique inflammatory or metabolic signatures, which may respond differently to treatment. This supports the need for standardized tools to identify these subgroups and develop personalized therapeutic strategies. Methods: This manuscript describes a standardized protocol for metabolomic and cytokine profiling of biological samples from ARDS patients. Specifically, we outline detailed procedures for the collection and processing of serum and bronchoalveolar lavage fluid, and for the subsequent multi-omic analysis. Metabolomic profiling is performed using gas chromatography–mass spectrometry (GC–MS), following a validated sample preparation and derivatization workflow, allowing both targeted and untargeted metabolic analysis. Cytokine profiling is conducted using a Luminex® multiplex immunoassay platform, enabling the simultaneous quantification of multiple inflammatory mediators from low-volume samples. The manuscript also provides recommendations on sample quality control, data integration with clinical and imaging parameters, and multivariate statistical approaches for data interpretation. Conclusions: The described approach enables high-throughput, standardized, and reproducible molecular profiling of ARDS patients across different clinical studies. It is intended to support the identification of ARDS subphenotypes based on inflammatory and metabolic signatures, and to foster the integration of biological data into personalized clinical decision-making. This may serve as a methodological foundation for future prospective investigations aimed at improving outcome prediction and tailoring therapy in patients with ARDS.","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"21 10","pages":"17-17"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147898887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"α7nAChR-mediated cholinergic anti-inflammatory pathway of immune cells in sepsis induced cardiac injury","authors":"","doi":"10.22514/sv.2025.003","DOIUrl":"https://doi.org/10.22514/sv.2025.003","url":null,"abstract":"Sepsis is a systemic syndrome characterized by widespread inflammatory responses induced by pathogenic microorganism invasion into the body, with increased suscep-tibility to major organs. Sepsis-induced cardiomyopathy is characterized by reversible myocardial depression or injury, primarily presenting as acute heart failure and/or arrhythmias triggered by sepsis. The mortality rate substantially increases when septic patients develop sepsis-induced cardiomyopathy. The cholinergic anti-inflammatory pathway (CAP) regulates inflammatory responses through the release of acetylcholine (ACh) via the vagus nerve and acts upon α7 nicotinic acetylcholine receptors (α7nAChR) on immune cells to suppress pro-inflammatory sytokines synthesis. In this review, we provide a concise overview of the current understanding of the α7nAChR-mediated CAP in sepsis-induced cardiac injury, with a primary focus on α7nAChR involvement in immune regulation.","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"21 1","pages":"21-21"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147919314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tormentic acid attenuates neuronal injury caused by ischemia-reperfusion via suppression of microglial mediated neuroinflammation","authors":"","doi":"10.22514/sv.2025.148","DOIUrl":"https://doi.org/10.22514/sv.2025.148","url":null,"abstract":"","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"21 10","pages":"107-107"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147901956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLF4 promotes sevoflurane-induced neurotoxicity by suppressing FOXO1 expression in neonatal rats","authors":"","doi":"10.22514/sv.2025.089","DOIUrl":"https://doi.org/10.22514/sv.2025.089","url":null,"abstract":"","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"21 6","pages":"111-111"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147904687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A year of impact: the best articles of 2024 in Signa Vitae","authors":"","doi":"10.22514/sv.2025.139","DOIUrl":"https://doi.org/10.22514/sv.2025.139","url":null,"abstract":"","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"21 10","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of ORM2 improves cerulein-induced acute pancreatitis in vitro via the p38 MAPK signaling pathway","authors":"","doi":"10.22514/sv.2024.160","DOIUrl":"https://doi.org/10.22514/sv.2024.160","url":null,"abstract":"The pathophysiology of acute pancreatitis remains poorly understood, and it is a severe inflammatory pancreatic disease that is becoming more widespread globally. The protein orosomucoid 2 (ORM2) is closely linked with tissue injury and inflammation. The purpose of this study was to investigate ORM2 expression in pancreatic acinar cells and its potential regulatory function in the regulation of inflammation and damage in acute pancreatitis. The model was established by culturing rat pancreatic acinar AR42J cells with 10 nM azuretin. Lentivirus was used to transfect AR42J cells to generate negative control and ORM2 knockdown cell lines. In order to track changes in ORM2 expression, cell proliferation, apoptosis, and the production of inflammatory cytokines in AR42J cells, this study carried out a number of tests. Western blotting showed expression changes in the p38 mitogen-activated protein kinases (MAPK) pathway. The results showed that ORM2 expression is up-regulated in acute pancreatitis in vitro, and knocking down ORM2 reversed the decrease in survival rate, the increase in apoptosis and the elevated inflammatory factor levels in AR42J cells induced by cerulein. Knockdown of ORM2 also inhibited the phosphorylation of p38 and extracellular signal-regulated kinase (ERK). In summary, ORM2 may significantly influence damage and inflammation in the in vitro rat pancreatic acinar cells model of acute pancreatitis by modulating the phosphorylation levels of p38 MAPK signaling.","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"20 12","pages":"93-93"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147888432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ursolic acid inhibits NLRP3 inflammasome activation and alleviates vascular smooth muscle injury in Kawasaki disease","authors":"Guoqing Chen, Yanru Wang, Ying Zhang, Fang Gu, Tong Yu","doi":"10.22514/sv.2024.041","DOIUrl":"https://doi.org/10.22514/sv.2024.041","url":null,"abstract":"Kawasaki disease (KD) is a kind of autoimmune disease with systemic vasculitis as the main pathological change. It is critical to explore potential new therapeutic agents to address KD disease and its complications. Ursolic acid (UA) is a pentacyclic triterpene (PT) carboxylic acid that has a number of important pharmacological activities, however, the possible effects of UA on the progression of KD and the mechanism are still unclear. Here we investigated the effects of UA on KD. We revealed that UA improved arterial injury in KD mice. UA improved vascular inflammation in KD mice. In addition, Ursolic suppressed NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome activation. We further found UA restrained vascular smooth muscle cell (VSMC) dedifferentiation, therefore suppressing KD progression. In summary, UA suppressed NLRP3 inflammasome activation as well as alleviated vascular smooth muscle injury in KD. We thought UA could act as a drug of KD.","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.signavitae.com/mre-signavitae/article/20240408-308/pdf/SV2023121301.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147910511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygonatum cyrtonema Hua Polysaccharides regulates NF-κB and Nrf2 pathways to alleviates oxidative stress and neuroinflammation in cerebral ischemia/reperfusion injury","authors":"","doi":"10.22514/sv.2024.162","DOIUrl":"https://doi.org/10.22514/sv.2024.162","url":null,"abstract":"Cerebral ischemia/reperfusion (I/R) injury is a leading cause of death and disability globally, particularly in China, and presents significant neurotoxic challenges despite timely revascularization. Polygonatum cyrtonema Hua polysaccharides (PCP) are well-known for their antioxidative, anti-inflammatory and immunomodulatory properties. This study aimed to address an unknown mechanism that regulates oxidative stress and neuroinflammation in cerebral ischemia/reperfusion injury induced by PCP. Our findings demonstrated that cell viability improved significantly when PCP was applied at concentrations of 20, 40 and 80 g/mL for 24 h in Oxygen and Glucose Deprivation/Reperfusion (OGD/R)-stimulated HT22 cells. PCP also markedly decreased Reactive Oxygen Species (ROS) and Malondialdehyde (MDA) levels by over 40% while enhancing Superoxide Dismutase (SOD) activity by approximately 35%. Additionally, PCP significantly reduced pro-inflammatory cytokines production, such as Tumor Necrosis Factor-alpha (TNF-α), Interleukin (IL)-1β and IL-6, by more than 50%. PCP activated the Nuclear factor erythroid 2-related factor 2 (Nrf2) axis and inhibited the Nuclear Factor kappa B (NF-κB) axis in HT22 cells under OGD/R conditions. Essentially, PCP modulates the oxidative stress and inflammation pathways to prevent injury induced by I/R. PCP may therefore be a promising treatment for ischemic stroke.","PeriodicalId":49522,"journal":{"name":"Signa Vitae","volume":"20 12","pages":"108-108"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147912300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}