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Carbon monoxide (CO) has shown various physiological effects including anti-inflammatory activity in several diseases, whereas the therapeutic efficacy of CO on sepsis-induced acute kidney injury (AKI) has not been reported as of yet. The purpose of the present study was to explore the effects of exogenous CO on sepsis-induced AKI and nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation in rats. Male rats were subjected to cecal ligation and puncture (CLP) to induce sepsis and AKI. Exogenous CO delivered from CO-releasing molecule 2 (CORM-2) was used intraperitoneally as intervention after CLP surgery. Therapeutic effects of CORM-2 on sepsis-induced AKI were assessed by measuring serum creatinine (Scr) and blood urea nitrogen (BUN), kidney histology scores, apoptotic cell scores, oxidative stress, levels of cytokines TNF-α and IL-1β, and NLRP3 inflammasome expression. CORM-2 treatment protected against the sepsis-induced AKI as evidenced by reducing serum Scr/BUN levels, apoptotic cells scores, increasing survival rates, and decreasing renal histology scores. Furthermore, treatment with CORM-2 significantly reduced TNF-α and IL-1β levels and oxidative stress. Moreover, CORM-2 treatment significantly decreased NLRP3 inflammasome protein expressions. Our study provided evidence that CORM-2 treatment protected against sepsis-induced AKI and inhibited NLRP3 inflammasome activation, and suggested that CORM-2 could be a potential therapeutic candidate for treating sepsis-induced AKI.

Abstract. The aim of the present study was to investigate the effect of intercostal nerve block combined with general anesthesia on the stress response and postoperative recovery in patients undergoing minimally invasive mitral valve surgery (MIMVS). A total of 30 patients scheduled for MIMVS were randomly divided into two groups (n=15 each): Group A, which received intercostal nerve block combined with general anesthesia and group B, which received general anesthesia alone. Intercostal nerve block in group A was performed with 0

The goal of this study was to establish a convenient and effective approach to anti-inflammation treatment by rebalancing the sympathetic-vagal system via vagal nerve stimulation (VNS). We established an endotoxemia model in Sprague-Dawley rats using lipopolysaccharide (LPS) injection. Electrical discharges in the vagal system, including the nucleus tractus solitarii (NTS) and afferent and efferent cervical vagal nerves, were detected. The condition of sympathetic-vagal balance, presented as heart rate variability (HRV) and hepatic norepinephrine/acetylcholine (NE/ACh), was measured following endotoxemia with and without VNS. Discharges in afferent and efferent vagal nerves increased significantly following LPS injection compared with the basis level and corresponding time points in the control group. Discharges in the NTS also increased significantly following LPS injection. The HRV components, including normalized high frequency (HFnm), normalized low frequency (LFnm), LF/HF, and very low frequency (VLF), increased significantly following LPS injection. HFnm values in the LPS + VNS group increased significantly compared with the LPS group. Conversely, LFnm, LF/HF, and VLF in the LPS + VNS group decreased significantly compared with the LPS group. Hepatic NE and ACh significantly decreased within 6 h after LPS injection compared with the basal level and the control groups (P < 0.05). VNS did not significantly improve hepatic NE, but the ACh levels in the LPS + VNS group were higher than those in other groups. Sympathetic and vagal nervous systems are enhanced following endotoxemia. The overexcitation of the sympathetic system leads to sympathetic-vagal disequilibrium. The rebalance of the sympathetic and vagal system is crucial for critically ill patients.

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Systematic manipulation of the reactivity of silicate materials in aqueous environment remains a challenging topic. Herein, by combining first-principles and reactive molecular dynamics simulations, we present a complete picture of the influence of impurity species on hydration reactivity, using the reactive triclinic tricalcium silicate phase as an example. We show that although initial hydration is influenced by the surface’s chemistry and structure, longer-term hydration is primarily controlled by proton transport through the bulk solid. Both shorter- and longer-term hydration processes are noted as being intrinsically correlated with electronic features. These outcomes provide the first direct evidence of the linkages between electronic structure and the longer-term (i.e., on the order of several nanoseconds) hydration behavior and sensitivity of hydrophilic crystalline materials and also offer a pathway to efficient compositional design for similar materials.

Inflammation plays an important role in cases of acute lung injury (ALI), and the Toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB) pathway, which can be regulated by Polygonatum sibiricum polysaccharides (PSPs), is closely related to the dynamics of lipopolysaccharide (LPS)-induced inflammation. Thus, we sought to evaluate whether or not PSPs prevent LPS-induced ALI by way of inhibiting inflammation via the TLR4/NF-κB pathway in rats. We established an ALI rat model by tracheal instillation of LPS, and by pre-injection of PSPs into rats to examine PSPs in the ALI rat model. We found that PSPs attenuated LPS-induced lung pathological changes in ALI rats, decreased LPS-induced myeloperoxidase (MOP) activity, and elevated malondialdehyde (MDA) levels in lung tissue. However, PSPs also decreased the LPS-induced increase in the neutrophil ratio, and decreased inflammatory factor levels in bronchoalveolar lavage fluid (BALF). Moreover, PSPs decreased LPS-induced increases in inflammatory factors measured by mRNA expression, and altered the levels of expression of TLR4, medullary differentiation protein 88 (Myd88), p-IKB-α/IKB-α and p-p65/p65 proteins in lung tissue. In vitro, PSPs also reduced apoptosis induced by LPS in BEAS-2B cells by suppressing inflammation through its effect of inhibiting the TLR4/NF-κB pathway. In conclusion, our results suggest that PSPs may be a potential drug for effective treatment of LPS-induced ALI, due to the ability to inhibit inflammation through effects exerted on the TLR4/Myd88/NF-κB pathway.

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