Polymer gels are a valuable class of polymeric materials that have recently attracted significant interest due to the exceptional properties such as versatility, soft-structure, flexibility and stimuli-responsive, biodegradability, and biocompatibility. Based on their properties, polymer gels can be used in a wide range of applications: food industry, agriculture, biomedical, and biosensors. The utilization of polymer gels in different medical and industrial applications requires a better understanding of the formation process, the factors which affect the gel’s stability, and the structure-rheological properties relationship. The present review aims to give an overview of the polymer gels, the classification of polymer gels’ materials to highlight their important features, and the recent development in biomedical applications. Several perspectives on future advancement of polymer hydrogel are offered.

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Polymer Gels: Classification and Recent Developments in Biomedical Applications

Sepsis is an abnormal condition with multiple organ dysfunctions caused by the uncontrolled infection response and one of the major diseases that seriously hang over global human health. Besides, sepsis is characterized by high morbidity and mortality, especially in intensive care unit (ICU). Among the numerous subsequent organ injuries of sepsis, myocardial injury is one of the most common complications and the main cause of death in septic patients. To better manage septic inpatients, it is necessary to understand the specific mechanisms of sepsis induced myocardial injury (SIMI). Therefore, this review will elucidate the pathophysiology of SIMI from the following certain mechanisms: apoptosis, mitochondrial damage, autophagy, excessive inflammatory response, oxidative stress and pyroptosis, and outline current therapeutic strategies and potential approaches in SIMI. 

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Research Progress on the Mechanism of Sepsis Induced Myocardial Injury

Acute myocardial infarction (AMI) is one of the most serious cardiovascular diseases with high morbidity and mortality. Numerous studies have indicated that S100A12 may has an essential role in the occurrence and development of AMI, and in-depth studies are currently lacking. The purpose of this study is to investigate the effect of S100A12 on inflammation and oxidative stress and to determine its clinical applicability in AMI. Here, AMI datasets used to explore the expression pattern of S100A12 in AMI were derived from the Gene Expression Omnibus (GEO) database. The pooled standard average deviation (SMD) was calculated to further determine S100A12 expression. The overlapping differentially expressed genes (DEGs) contained in all included datasets were recognized by the GEO2R tool. Then, functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were carried out to determine the molecular function of overlapping DEGs. Gene set enrichment analysis (GSEA) was conducted to determine unrevealed mechanisms of S100A12. Summary receiver operating characteristic (SROC) curve analysis and receiver operating characteristic (ROC) curve analysis were carried out to identify the diagnostic capabilities of S100A12. Moreover, we screened miRNAs targeting S100A12 using three online databases (miRWalk, TargetScan, and miRDB). In addition, by comprehensively using enzyme-linked immunosorbent assay (ELISA), real-time quantitative PCR (RT–qPCR), Western blotting (WB) methods, etc., we used the AC16 cells to validate the expression and underlying mechanism of S100A12. In our study, five datasets related to AMI, GSE24519, GSE60993, GSE66360, GSE97320, and GSE48060 were included; 412 overlapping DEGs were identified. Protein-protein interaction (PPI) network and functional analyses showed that S100A12 was a pivotal gene related to inflammation and oxidative stress. Then, S100A12 overexpression was identified based on the included datasets. The pooled standard average deviation (SMD) also showed that S100A12 was upregulated in AMI (SMD = 1.36, 95% CI: 0.70-2.03, p = 0.024). The SROC curve analysis result suggested that S100A12 had remarkable diagnostic ability in AMI (AUC = 0.90, 95% CI: 0.87-0.92). And nine miRNAs targeting S100A12 were also identified. Additionally, the overexpression of S100A12 was further confirmed that it maybe promote inflammation and oxidative stress in AMI through comprehensive in vitro experiments. In summary, our study suggests that overexpressed S100A12 may be a latent diagnostic biomarker and therapeutic target of AMI that induces excessive inflammation and oxidative stress. Nine miRNAs targeting S100A12 may play a crucial role in AMI, but further studies are still needed. Our work provides a positive inspiration for the in-depth study of S100A12 in AMI.

/pdf/inflammation-and-oxidative-stress-role-of-s100a12-as-a-2zmz8pcm.pdf

Inflammation and Oxidative Stress Role of S100A12 as a Potential Diagnostic and Therapeutic Biomarker in Acute Myocardial Infarction

Abstract Sepsis is an abnormal condition with multiple organ dysfunctions caused by the uncontrolled infection response and one of the major diseases that seriously hang over global human health. Besides, sepsis is characterized by high morbidity and mortality, especially in intensive care unit (ICU). Among the numerous subsequent organ injuries of sepsis, myocardial injury is one of the most common complications and the main cause of death in septic patients. To better manage septic inpatients, it is necessary to understand the specific mechanisms of sepsis induced myocardial injury (SIMI). Therefore, this review will elucidate the pathophysiology of SIMI from the following certain mechanisms: apoptosis, mitochondrial damage, autophagy, excessive inflammatory response, oxidative stress and pyroptosis, and outline current therapeutic strategies and potential approaches in SIMI.

https://www.dovepress.com/getfile.php?fileID=82421

Histone deacetylase 4 (HDAC4) modulates immunity, inflammation, and osteoblast differentiation to engage in rheumatoid arthritis (RA) etiology. This study aimed to evaluate the HDAC4 longitudinal change and its relationship with clinical features and outcomes in RA patients.

Serum HDAC4 level in rheumatoid arthritis: Longitudinal change during treatment and correlation with clinical outcomes

Sepsis-induced cardiac dysfunction can lead to death in sepsis. In this case, we targeted to explore in detail the relative mechanism of microRNA (miR)-124-3p in sepsis-induced myocardial injury via the specific protein 1/histone deacetylase 4/hypoxia-inducing factor 1α (SP1/HDAC4/HIF-1α) axis. Septic rats were modeled by cecal ligation puncture while in vitro septic cardiomyocyte H9C2 were induced by lipopolysaccharide (LPS). miR-124-3p/SP1/HDAC4/HIF-1α expression levels in myocardial tissues of septic rats and LPS-treated H9C2 cells were measured. miR-124-3p overexpression and SP1 silencing assays were implemented on LPS-treated H9C2 cells to explore theirs actions in inflammation, oxidative stress and cell apoptosis. The interactions of miR-124-3p, SP1, and HDAC4 were testified. miR-124-3p was lowly expressed while SP1, HDAC4, and HIF-1α were highly expressed in sepsis. Upregulation of miR-124-3p ameliorated inflammation, oxidative stress, and apoptosis of LPS-treated H9C2 cells. Silencing SP1 improved LPS-induced damage to cardiomyocytes. miR-124-3p targeted SP1 and HDAC4 interacted with SP1. SP1 overexpression antagonized miR-124-3p upregulation-induced improvements in LPS-induced cardiomyocyte damage. This study illustrates that miR-124-3p improves myocardial injury in septic rats through targeted regulation of SP1 to mediate HDAC4/HIF-1α. 

/pdf/microrna-124-3p-attenuates-myocardial-injury-in-sepsis-via-26h2zr5y.pdf

microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis

/pdf/microrna-124-3p-attenuates-myocardial-injury-in-sepsis-via-3tm3d2qy.pdf

Introduction Acute lung injury (ALI) is a major cause of morbidity and mortality after intestinal ischaemia/reperfusion (I/R). The gut microbiota and its metabolic byproducts act as important modulators of the gut–lung axis. This study aimed to define the role of succinate, a key microbiota metabolite, in intestinal I/R-induced ALI progression. Methods Gut and lung microbiota of mice subjected to intestinal I/R were analysed using 16S rRNA gene sequencing. Succinate level alterations were measured in germ-free mice or conventional mice treated with antibiotics. Succinate-induced alveolar macrophage polarisation and its effects on alveolar epithelial apoptosis were evaluated in succinate receptor 1 (Sucnr1)-deficient mice and in murine alveolar macrophages transfected with Sucnr1-short interfering RNA. Succinate levels were measured in patients undergoing cardiopulmonary bypass, including intestinal I/R. Results Succinate accumulated in lungs after intestinal I/R, and this was associated with an imbalance of succinate-producing and succinate-consuming bacteria in the gut, but not the lungs. Succinate accumulation was absent in germ-free mice and was reversed by gut microbiota depletion with antibiotics, indicating that the gut microbiota is a source of lung succinate. Moreover, succinate promoted alveolar macrophage polarisation, alveolar epithelial apoptosis and lung injury during intestinal I/R. Conversely, knockdown of Sucnr1 or blockage of SUCNR1 in vitro and in vivo reversed the effects of succinate by modulating the phosphoinositide 3-kinase-AKT/hypoxia-inducible factor-1α pathway. Plasma succinate levels significantly correlated with intestinal I/R-related lung injury after cardiopulmonary bypass. Conclusion Gut microbiota-derived succinate exacerbates intestinal I/R-induced ALI through SUCNR1-dependent alveolar macrophage polarisation, identifying succinate as a novel target for gut-derived ALI in critically ill patients. Succinate accumulation in the lungs is associated with the imbalance of succinate-producing and -consuming bacteria in the gut during intestinal ischaemia/reperfusion. Lung injury was exacerbated by succinate via alveolar macrophage polarisation. https://bit.ly/3fTR9AM

Gut microbiota-derived succinate aggravates acute lung injury after intestinal ischaemia/reperfusion in mice

ABSTRACT Introduction: Myocardial ischemia-reperfusion (I/R) injury is one of the mechanisms contributing to the high mortality rate of acute myocardial infarction. Purpose: This study intended to study the role of naringin in cardiac I/R injury. Methods: AC16 cells (human cardiomyocyte cell line) were subjected to oxygen-glucose deprivation/recovery (OGD/R) treatment and/or naringin pretreatment. Then, the apoptosis was examined by flow cytometry and Western blotting. The concentration of IL-6, IL-8 and TNF-α was measured by enzyme-linked immunosorbent assay (ELISA) kits. How naringin influenced microRNA expression was examined by microarrays and quantitative real-time polymerase chain reaction (qRT-PCR). Dual luciferase reporter assay was employed to evaluate the interaction between miR-126 and GSK-3β. The GSK-3β/β-catenin signaling pathway was examined by Western blotting. Finally, rat myocardial I/R model was created to examine the effects of naringin in vivo. Results: Naringin pretreatment significantly decreased the cytokine release and apoptosis of cardiomyocytes exposed to OGD/R. Bioinformatical analysis revealed that naringin upregulated miR-126 expression considerably. Also, it was found that miR-126 can bind GSK-3β and downregulate its expression, suggesting that naringin could decrease GSK-3β activity. Next, we discovered that naringin increased β-catenin activity in cardiomyocytes treated with OGD/R by inhibiting GSK-3β expression. Our animal experiments showed that naringin pre-treatment or miR-126 agomir alleviated myocardial I/R. Conclusions: Naringin preconditioning can reduce myocardial I/R injury via regulating miR-126/GSK-3β/β-catenin signaling pathway, and this chemical can be used to treat acute myocardial infarction.

/pdf/naringin-attenuates-acute-myocardial-ischemia-reperfusion-elltc0z1.pdf

Naringin attenuates acute myocardial ischemia-reperfusion injury via miR- 126/GSK-3β/β-catenin signaling pathway

Local anesthetic effects of lidocaine-loaded carboxymethyl chitosan cross-linked with sodium alginate hydrogels for drug delivery system, cell adhesion, and pain management

Mei Wu

Papers

microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis

microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis

Gut microbiota-derived succinate aggravates acute lung injury after intestinal ischaemia/reperfusion in mice

Naringin attenuates acute myocardial ischemia-reperfusion injury via miR- 126/GSK-3β/β-catenin signaling pathway

Local anesthetic effects of lidocaine-loaded carboxymethyl chitosan cross-linked with sodium alginate hydrogels for drug delivery system, cell adhesion, and pain management