The mortality rate of sepsis-associated disseminated intravascular coagulation (DIC) is high. This study aimed to explore the efficacy of therapeutic plasma exchange (TPE) in sepsis-associated DIC patients by improving endothelial function. A total of 112 sepsis-associated DIC patients were randomly divided into the TPE group (n = 40), the heparin (HP) group (n = 36), and the SHAM group (n = 36). The SHAM group received conventional treatment; the HP group was treated with HP based on conventional treatment; and the TPE group received conventional treatment plus TPE. The differences in thromboelastogram (TEG), platelet (PLT), coagulation function, and the endothelial cell (EC) injury biomarkers at 6 h, 24 h, 48 h, 72 h, and 7 days after TPE were compared among the three groups, and the three groups were compared in terms of Acute Physiology and Chronic Health Evaluation II (APACHE II) score, Sepsis-Related Organ Failure Assessment (SOFA) score, the length of intensive care unit (ICU) hospitalization, 28-day mortality rate, 28-day cumulative survival rate, the incidence of bleeding events, the incidence of acute kidney injury (AKI), and acute respiratory distress syndrome (ARDS). The efficacy of TPE is superior to the HP in increasing PLT, improving coagulation function, increasing the 28-day cumulative survival rate, and reducing the length of ICU hospitalization, 28-day mortality, and the incidence of bleeding events, AKI, and ARDS with statistically significant differences ( P  < .05). Moreover, the effect of TPE outperforms HP on the EC injury biomarkers with statistically significant differences ( P  < .05). Our results suggest that TPE may be more effective than HP in the treatment of patients with sepsis-associated DIC. The possible mechanism is via improving endothelial function.

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Sepsis is an emergency systemic illness caused by pathogen infection and the combined result of the underactivity and overactivity of a patient's own immune system. However, the molecular mechanism of this illness remains largely unknown. Lipopolysaccharide (LPS) was injected to establish a sepsis model, and heart tissue was used to analyze transcriptome changes in mice. LPS injection was used to develop a sepsis model, which resulted in cardiac tissue rearrangement and inflammatory response activation. An RNA-sequencing-based transcriptome assay using mouse heart tissue with or without LPS injection showed that 3,326 and 1,769 genes were upregulated and downregulated, respectively (>2-fold changes; P<0.05). Furthermore, these differentially expressed genes were classified into 20 pathways, including 'Wnt signaling pathway', 'VEGF signaling pathway' and 'TGF-β signaling pathway', and these altered genes were enriched in 41 Gene Ontology terms. The application of Wnt3a inhibited the activation of the LPS-induced inflammatory response and activated Wnt signaling, as well as protecting against LPS-mediated cardiac tissue damage in mice. In contrast, inhibition of Wnt signaling by injection of its inhibitor IWR induced plasminogen activator inhibitor-1 expression and resulted in cardiac structure derangement, which was similar to the symptoms caused by injection of LPS, suggesting that LPS-induced damage to heart tissue may be via inhibition of Wnt signaling. The present analyses showed that Wnt signaling serves a pivotal role in sepsis development and may improve our understanding of the molecular basis underlying sepsis.

Objective: This study aimed to investigate whether the antihypertensive effect of irbesartan (IRB) in spontaneously hypertensive rats (SHR) was achieved through improvement of insulin resistance and adjustment of the LPN–APN imbalance.Methods:SHR rats were divided into SHAM, SHR-A and SHR-I group(8 per group). Homologous Wistar–Kyoto (WKY) rats were used as control group (WKY).The SHR-I group received 30 mg/kg/d IRB, the SHR-A group received 2.5 mg/kg AML. After 8 weeks, systolic blood pressure (SBP) was measured. The concentrations of blood glucose, insulin, LPN and APN were detected. Rat epididymal adipose tissues were collected to analyze the mRNA expression levels ofepididymal LPN and APN using reverse transcription–polymerase chain reaction. In addition, the LPN/APN ratio was calculated. Results:SBP, homeostasis model assessment of insulin resistance (HOMA-IR), LPN concentration, adipose LPN mRNA expression level, and the LPN/APN ratio increased ( P <0.05) and APN concentration and adipose APN mRNA expression level decreased ( P <0.05) in SHR rats.IRB decreased SBP, HOMA-IR, serum LPN, adipose LPN mRNA expression, and the LPN/APN ratio and increased serum APN and adipose APN mRNA expression. Conclusion: The antihypertensive effect of IRB in SHR rats was associated with its improvement of insulin resistance and correction of the LPN–APN imbalance. Abbreviations: ANOVA, one-way analysis of variance; SHR, Spontaneously hypertensive rats; WKY, Wistar kyoto rats; IRB, Irbesartan; AML, Amlodipine; LPN, Leptin; APN, Adiponectin; Ang-II, AngiotensinⅡ; HOMA-IR, Homoeostasis model assessment-insulin resistance; SBP, Systolic blood pressure; RT-PCR, Reverse transcription polymerase chain reaction; ARB, AngiotensinⅡreceptor blocker