OBJECTIVETo investigate the effect of seawater exposure on intestinal injury in rabbits with scald burns and explore the mechanisms.

METHODSSixty-three rabbits with scald burns covering 20% total body surface area were randomized equally into scald control group (group A), scald with freshwater exposure group (group B), and scald with seawater exposure group (group C). At 2, 4 and 8 h after scald burns, 7 rabbits from each group were sacrificed for detecting plasma superoxide dismutase (SOD) and lipid peroxide (LPO) levels and intestinal contents of prostaglandins (PGs) and for examining the intestinal pathologies; immunohistochemistry was used to detect the expression of Bax and Bcl-2 proteins in the small intestinal epithelium.

RESULTSThe rabbits in group C showed severer intestinal mucosal and barrier function damages than those in groups A and B. The plasma SOD activity and intestinal PGs contents were significantly lowered in group C than in groups A and B at 2, 4, and 8 h postburn (P<0.01) and reduced as the postburn time extended (P<0.01). In group C, plasma LPO content was the highest among the groups (P<0.01) and increased significantly with the seawater exposure time (P<0.01). The expression of Bax and Bcl-2 in the intestinal mucosal tissues was also the highest in group C (P<0.01) at 4 h and 8 h postburn and increased significantly with time (P<0.01).

CONCLUSIONSeawater exposure exacerbates scald burn-induced intestinal mucosal and barrier function damages in rabbits mainly by aggravating intestinal inflammation and structural damage, as evidenced by decreased intestinal PGs contents and plasma SOD activity, increased plasma PLO content, and enhanced Bax and Bcl-2 protein expressions in the intestinal mucosa.

Animals ; Burns ; pathology ; Intestinal Mucosa ; metabolism ; physiopathology ; Lipid Peroxidation ; Prostaglandins ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rabbits ; Seawater ; adverse effects ; Soft Tissue Injuries ; Superoxide Dismutase ; blood ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo investigate the effect of antibacterial peptide LL-37 on the integrity of Acinetobacter baumannii biofilm.

METHODSA model of Acinetobacter baumannii biofilm in vitro was constructed by plates and crystal violet staining method, and the minimal inhibitory concentration of LL-37 was determined by broth dilution. The biofilm morphology was observed by scanning electron microscopy and biofilm formation was analyzed by the crystal violet staining of the adherent biofilm in the presence of antibacterial peptide LL-37.

RESULTSIn the Acinetobacter baumannii biofilm model, the minimal inhibitory concentration of LL-37 was 64 µg/ml; LL-37 caused structural damage of the biofilm at a low concentration of 2.5 µg/ml. The biofilm was decreased gradually as the concentration of LL-37 increased.

CONCLUSIONLL-37 even at a concentration far below its minimal inhibitory concentration can cause structural damage of Acinetobacter baumannii biofilm in vitro.

Acinetobacter baumannii ; drug effects ; physiology ; Biofilms ; drug effects ; Cathelicidins ; pharmacology ; Microbial Sensitivity Tests

OBJECTIVETo screen the genes related with leukocyte responses in mice early after burn injury by bioinformatic analysis of the gene expression profiling data.

METHODSGene expression profiles were obtained from GEO (GSE7404, Mouse musculus, 25% TBSA, full-thickness) database. After screening of the differentially expressed genes (DEGs) through paired-sample t-test and fold-change, DAVID online tools were used to select the DEGs related to leukocyte responses to burns by GO functional enrichment analysis; the interacting genes identified through KEGG pathway enrichment analysis were transferred to STRING to construct the protein-protein interaction (PPI) network. Biological annotation of the sub-networks was executed using the software Cytoscape. Real-time PCR was used to verify the DEGs identified in mice.

RESULTSOf the 259 leukocyte response-related DEGs screened at 1 day post-burn, 118 were up-regulated and 141 were down-regulated. KEGG pathway enrichment analysis showed that the pathways were associated with the immune function, cell growth and cell death. PPI network and module analysis suggested that some of genes (such as Lck, Stat1, Myd88, Stat3, and Jun) play critical roles in the PPI network post-burn. RT-PCR results were consistent with those of bioinformatic analysis.

CONCLUSIONSLck, Stat1, Myd88, Stat3, and Jun might be critical players in the development of leukocyte response in mice early after burn injury. Our finding provides new insights into the pathogenesis of leukocyte response to burn injury and identifies several potential biomarkers for burn treatment.

Animals ; Burns ; genetics ; Computational Biology ; Down-Regulation ; Gene Expression Profiling ; Gene Regulatory Networks ; Leukocytes ; physiology ; Mice ; Real-Time Polymerase Chain Reaction ; Software ; Up-Regulation

Ischemic stroke (IS) is a severe cerebrovascular disease with a high incidence, mortality, and disability rate. The first-line treatment for IS is the use of recombinant tissue plasminogen activator (r-tPA). Regrettably, numerous patients encounter delays in treatment due to the narrow therapeutic window and the associated risk of hemorrhage. Traditional Chinese medicine (TCM) has exhibited distinct advantages in preventing and treating IS. TCM enhances cerebral microcirculation, alleviates neurological disorders, regulates energy metabolism, mitigates inflammation, reduces oxidative stress injuries, and inhibits apoptosis, thereby mitigating brain damage and preventing IS recurrence. This article summarizes the etiology, pathogenesis, therapeutic strategies, and relationship with modern biology of IS from the perspective of TCM, describes the advantages of TCM in the treatment of IS, and further reviews the pharmacodynamic characteristics and advantages of TCM in the acute and recovery phases of IS as well as in post-stroke complications. Additionally, it offers valuable insights and references for the clinical application of TCM in IS prevention and treatment, as well as for the development of novel drugs.

OBJECTIVE: To compare 3 commonly used methods for drug delivery via the lumbar spinal subarachnoid space in rats. METHODS: We compared the effects of 3 methods for drug delivery via the lumbar spinal subarachnoid space in Sprague Dawley rats, namely acute needle puncture, chronic catheterization via laminectomy, and non-laminectomized catheterization. Body weight changes of the rats were measured, and their general and neurological conditions were assessed after the surgeries. The motor function of the rats was examined using rota rod test both before and after the surgeries. Nociceptive tests were performed to assess nociception of the rats. HE staining was used to examine local inflammation caused by the surgeries in the lumbar spinal cord tissue, and lidocaine paralysis detection and toluidine blue dye assay were used to confirm the precision of drug delivery using the 3 methods. RESULTS: Both needle puncture and catheterization via laminectomy resulted in a relatively low success rate of surgery and caused neurological abnormalities, severe motor dysfunction, hyperalgesia, allodynia and local inflammation. Catheterization without laminectomy had the highest success rate of surgery, and induced only mild agitation, slight cerebral spinal fluid leakage, mild sensory and motor abnormalities, and minimum pathology in the lumbar spinal cord. Catheterization without laminectomy produced less detectable effects on the behaviors in the rats and was well tolerated compared to the other two methods with also higher precision of drug delivery. CONCLUSIONS Catheterization without laminectomy is a safe, accurate and effective approach to lumbar drug delivery in rats.

Cognitive dysfunction is one of the common central nervous systems (CNS) complications of diabetes mellitus, which seriously affects the quality of life of patients and results in a huge economic burden. The glymphatic system dysfunction mediated by aquaporin-4 (AQP4) loss or redistribution in perivascular astrocyte endfeet plays a crucial role in diabetes-induced cognitive impairment (DCI). However, the mechanism of AQP4 loss or redistribution in the diabetic states remains unclear. Accumulating evidence suggests that peripheral insulin resistance target tissues and CNS communication affect brain homeostasis and that exosomal miRNAs are key mediators. Glucose and lipid metabolism disorder is an important pathological feature of diabetes mellitus, and skeletal muscle, liver and adipose tissue are the key target insulin resistance organs. In this review, the changes in exosomal miRNAs induced by peripheral metabolism disorders in diabetes mellitus were systematically reviewed. We focused on exosomal miRNAs that could induce low AQP4 expression and redistribution in perivascular astrocyte endfeet, which could provide an interorgan communication pathway to illustrate the pathogenesis of DCI. Furthermore, the mechanisms of exosome secretion from peripheral insulin resistance target tissue and absorption to the CNS were summarized, which will be beneficial for proposing novel and feasible strategies to optimize DCI prevention and/or treatment in diabetic patients.