Background: Inflammation is one of the causes of neuroblastoma progression. Propofol attenuates inflammation by repressing nuclear transcription factor κB (NF-κB) in different diseases. But its effect on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced inflammation is not known. Objective: This study investigated the role and mechanism of action of propofol on OGD/Rinduced inflammation in mouse N2A neuroblastoma cells. Methods: MTT was performed on mouse neuroblastoma cells N2A to assess and select the maximum safe dose of propofol. Next, N2A cells were pretreated with propofol and then, exposed to the OGD condition for 3 h and reoxygenated for 6 h. The content of the inflammatory factors, interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α), in the medium was measured by ELISA, while their protein expression was detected by western blot and immunofluorescence. The protein expression of P65, p-P65, IKBα and p-IKBα belonging to the NF-κB pathway was also determined by western blot in N2A cells. To further confirm the mechanism of propofol on OGD/R-induced inflammation in mouse N2A cells, P65 was over-expressed and the above experiments were repeated. Results: Propofol did not affect cell viability of N2A cells even at the maximum concentration used (30 µM), thus, 30 µM of propofol was selected to perform our experiments. Besides, OGD/R induced inflammation and activation of NF-κB pathway with increased p-P65 and p-IKBα expression, and propofol pretreatment inhibited OGD/R induced inflammation and activation of NF-κB pathway in N2A cells. Over-expression of P56 abolished the effects of propofol on OGD/Rinduced inflammation and activation of NF-κB pathway in N2A cells. Conclusion: Our work demonstrated for the first time that propofol pretreatment ameliorated OGD/R induced inflammation via NF-κB pathway modulation in mouse neuroblastoma N2A cells, indicating that propofol might be considered as a potential therapeutic approach to reduce inflammation in neuroblastoma.

Abstract. The ultrasound probe and advancement of the needle during real-time ultrasound-assisted guidance of catheterization of the right internal jugular vein (RIJV) tend to collapse the vein, which reduces the success rate of the procedure. We have developed a novel puncture point-traction method (PPTM) to facilitate RIJV cannulation. The present study examined whether this method facilitated the performance of RIJV catheterization in anesthetized patients. In this study, 120 patients were randomly assigned to a group in which PPTM was performed (PPTM group, n=60) or a group in which it was not performed (non-PPTM group, n=60). One patient was excluded because of internal carotid artery puncture and 119 patients remained for analysis. The cross-sectional area (CSA), anteroposterior diameter (AD) and transverse diameter (TD) of the RIJV at the cricoid cartilage level following the induction of anesthesia and during catheterization were measured, and the number with obvious loss of resistance (NOLR), the number with easy aspiration of blood into syringe (NEABS) during advancement of the needle, and the number of first-pass punctures (NFPP) during catheterization were determined. In the non-PPTM group, the CSA was smaller during catheterization compared with that following the induction of anesthesia (P<0.01). In the PPTM group compared with the non-PPTM group during catheterization, the CSA was larger (P<0.01) and the AD (P<0.01) and TD (P<0.05) were wider; NOLR (P<0.01), NEABS (P<0.01) and NFPP (P<0.01) increased significantly. The findings from this study confirmed that the PPTM facilitated catheterization of the RIJV and improved the success rate of RIJV catheterization in anesthetized patients in the supine position.

Objective. To explore the effect and possible mechanism of sufentanil on sepsis-induced myocardial injury and stress response in rats. Methods. The cecal ligation and puncture (CLP) method was utilized to establish the sepsis model of rats to explore the effect of sufentanil pretreatment with different concentrations on myocardial injury and oxidative stress in CLP rats. Echocardiogram was applied for detecting cardiac hemodynamic parameters in rats; hematoxylin and eosin (HE) staining as well as TUNEL staining was done for observing pathological changes of myocardial tissue and cardiomyocyte apoptosis in rats, respectively; biochemical testing and enzyme-linked immunosorbent assay (ELISA) were done for determining myocardial injury marker level in serum, oxidative stress substances in myocardial tissue, and neuroendocrine hormone level in serum of rats, respectively; finally, Western blot was performed for checking the expression level of ERK/GSK-3β signaling pathway-related proteins in myocardial tissue of rats. Results. A model of rat with sepsis-induced myocardial injury was constructed with the CLP method. Specifically, this rat model was characterized by obvious cardiac function and tissue damage, cardiomyocyte apoptosis, and oxidative stress response. Sufentanil pretreatment significantly improved cardiac function injury, alleviated pathological injury and oxidative stress response in myocardial tissue, and inhibited cardiomyocyte apoptosis. Specifically, after sufentanil pretreatment, left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) were downregulated, and left ventricular ejection fraction (LVEF) was upregulated; the level of B-type natriuretic peptide (BNP) of serum, creatine kinase isoenzyme (CK-MB), and troponin (cTnl) decreased; besides, malondialdehyde (MDA) level was declined, while activities of superoxide dismutase (SOD) and catalase (CAT) were increased. What is more, further mechanism exploration also revealed that sufentanil could reverse the activity of the sepsis-induced ERK/GSK-3β signaling pathway. Conclusion. Sufentanil has an obvious protective effect on myocardial injury and stress response in CLP rats, and this protective effect may be related to the activation of the ERK/GSK-3β signaling pathway.

Background: The aim of this study was to systematically evaluate the efficiency of propofol versus isoflurane anesthesia interventions in treating elderly patients with postoperative cognitive dysfunction. Methods: We performed an in-depth search in the PubMed, EMBASE, Cochrane Library, Chongqing VIP, WanFang, China National Knowledge Infrastructure, and SinoMed. Additionally, we reviewed the reference lists of included studies. Two independent authors examined the quality of the study and the quality of the extracted data. Regarding the dichotomous outcomes, we stated the results as relative risk, with 95% confidence intervals. We further expressed incessant outcomes as mean difference with a confidence level of 95%. Results: The findings of the study will be published in a peer-reviewed journal. Conclusion: Findings of this study will help in providing insight to establish if propofol is a suitable intervention to treat postoperative cognitive dysfunction in elderly patients. Systematic review registration number: INPLASY202090042

Purpose: To investigate the effect of dexmedetomidine in a rat model of acute lung injury (ALI), and the underlying mechanism. Methods: Acute lung injury (ALI) was induced in adult male Sprague Dawley rats (n = 27) using lipopolysaccharide (LPS). Three rat groups were used (9 rats/group): untreated control, LPS and treatment groups. Pathological lesions in rat pulmonary tissues were assessed and inflammatory scores determined. The levels TNF-α and IL-6 in BALF were determined using their respective enzyme-linked immunosorbent assay (ELISA) kits, while protein levels of p-IκB and NF-κB p65 were assessed by Western blotting. Results: Lung tissue damage was markedly mitigated in treatment mice, relative to LPS mice (p < 0.05). Inflammatory scores and population of neutrophils and macrophages increased significantly in LPS mice, relative to control, but decreased by dexmedetomidine exposure (p < 0.05). Similarly, TNF-α and IL-6 levels in pulmonary tissue homogenates of LPS rats were increased, relative to control rats, but were downregulated by dexmedetomidine exposure (p < 0.05). Moreover, dexmedetomidine downregulated the expressions of p-IκB and NF-κB p65 in pulmonary tissues (p < 0.05). Conclusion: Dexmedetomidine mitigates LPS-induced ALI in rats by blocking the activation of NF-κB and IκB, coupled with inhibition of the secretion of TNF-α and IL-6. Keywords: Acute lung injury, Dexmedetomidine, Inflammatory cytokines, NF-κB pathway, Sepsis