Novel cellulose/montmorillonite mesoporous composite beads for dye removal in single and binary systems.

Fine aminated cellulose/montmorillonite mesoporous composite beads (ACeMt) were prepared as green-based adsorbent via a novel approach utilizing ultra-fine calcium carbonate as a pore-forming agent to increase the porosity and specific surface area of ACeMt. The resulting bioadsorbent was characterized by means of SEM, FTIR and BET analysis and used for dye removal. Adsorption experimental data were fitted with various isotherm and kinetic models. The results indicated that chemical adsorption was the rate-limiting step. The maximum adsorption capacities of ACeMt, better described by Langmuir model, were much higher than those of conventional adsorbents, particularly for the removal of Auramine O dye (up to 1336.2 mg/g at 55 °C). The adsorptions at equilibrium were better correlated with Redlich-Peterson model and uncompetitive Langmuir isotherm model in single and binary system, respectively. Overall, ACeMt is a promising bioadsorbent and highly efficient in the removal of dyes for water clarification.

Activation of astrocytes and expression of inflammatory cytokines in rats with experimental autoimmune encephalomyelitis.

The aim of the study was to investigate and discuss the activation of astrocytes and the expression of inflammatory cytokines in rats with experimental autoimmune encephalomyelitis (EAE). Twenty Wistar rats were randomly divided into the normal control (n=10) and EAE group (n=10). The rats in the EAE group were injected intraperitoneally with myelin oligodendrocyte glycoprotein 35-55 emulsion, and those in the control group were injected with the equivalent volume of normal saline. Wear neurological function scale was applied to evaluate the neurological functions of the rats, and the weight changes were recorded. At 21 days after immunization, hematoxylin and eosin staining was used to detect the histomorphology, and immunofluorescence was used to measure the activation conditions of the brain astrocytes. Reverse transcription-polymerase chain reaction and western blot analysis were utilized to detect the messenger RNA (mRNA) and protein levels of inflammatory factors. The disease occurred in rats of the EAE group at 9 days after immunization, and the incidence rate was 80%. The Wear score of the rats in the EAE group was significantly increased compared with that in the control group (P<0.05). At 9 days after immunization, the weight of the rats in the EAE group was obviously lower than that in the control group (P<0.05). The inflammatory lesion of rats in the EAE group mainly occurred in the region of brain parenchyma. The glial fibrillary acidic protein level in the brain sections of the rats in the EAE group was markedly elevated compared with that in control group. The mRNA and protein levels of interleukin-10 in the rat brain in EAE group were decreased notably (P<0.05), while those of interferon-γ and tumor necrosis factor-α were increased significantly (P<0.05). The significant increases in the activation level of astrocytes and inflammatory cytokine level have a close relationship with EAE progression.

Effects of silencing the DUSP1 gene using lentiviral vector-mediated siRNA on the release of proinflammatory cytokines through regulation of the MAPK signaling pathway in mice with acute pancreatitis.

The present study investigated the effects of dual specificity phosphatase 1 (DUSP1) gene silencing using lentiviral vector-mediated small interfering (si)RNA on the release of proinflammatory cytokines through the regulation of the mitogen­activated protein kinase (MAPK) signaling pathway in mice with acute pancreatitis (AP). Two siRNA­DUSP1 sequences and one scramble siRNA sequence were designed, and the expression of DUSP1 was detected using western blot analysis to screen for the one with a higher interference rate. An AP mouse model was established, and KM mice were assigned to either a control, siRNA, AP, AP+PD98059, AP+scramble, AP+siRNA or AP+PD98059+siRNA group. The expression of proinflammatory cytokines, including tumor necrosis factor (TNF)­α, interleukin (IL)­1ß and IL­6, high mobility group box 1 (HMGB1), and S100A12 in serum samples were detected using an enzyme­linked immunosorbent assay at 12, 24 and 48 h post­modeling. The serum amylase levels were also detected. The expression levels of DUSP1, TNF­α, IL­1ß, IL­6, HMGB1, S100A12, phosphorylated (p­) extracellular signal­regulated kinase (ERK), p­c­Jun N­terminal kinase (JNK), p­p38, ERK, JNK and p38 in pancreatic, liver, kidney and lung tissues were detected using reverse transcription­quantitative polymerase chain reaction and western blot analysis. Compared with the control group, the siRNA group demonstrated marginally upregulated serum amylase, lipase, urinary trypsinogen­2, and proinflammatory cytokines, HMGB1 and S100A12 in serum and tissues, with no statistically significant difference, elevated expression levels of p­ERK, p­JNK and p­p38, and decreased expression of DUSP1. The other five groups demonstrated increased expression levels of TNF­α, IL­1ß, IL­6, HMGB1, S100A12, amylase, lipase and urinary trypsinogen­2 in serum, and increased expression levels of DUSP1, TNF­α, IL­1ß, IL­6, HMGB1, S100A12, p­ERK, p­JNK and p­p38 in tissues. Compared with the AP group, the AP+PD98059+siRNA group had decreased expression of DUSP1 in tissues, whereas the AP+PD98059 group had decreased serum expression levels of TNF­α, IL­1ß, IL­6, HMGB1, S100A12 and amylase, lipase and urinary trypsinogen­2. The expression levels of TNF­α, IL­1ß, IL­6, HMGB1, S100A12, p­ERK, p­JNK, p­p38 in tissues, and edema of pancreatic tissue were alleviated, whereas the opposite results were observed in the AP+siRNA group with the decreased expression of DUSP1. The results suggested that DUSP1 gene silencing promoted the release of proinflammatory cytokines through activation of the MAPK signaling pathway in mice with AP.

Protective Role of TNIP2 in Myocardial Injury Induced by Acute Pancreatitis and Its Mechanism.

BACKGROUND Aberrant regulation of nuclear factor-κB (NF-κB) and the signaling pathways that regulate its activity have been found to be involved in various pathologies, particularly cancers, as well as inflammatory and autoimmune diseases. Acute pancreatitis (AP) is a complex pathological process, depending on autodigestion caused by premature activation of zymogens. This study aimed to investigate the effect of high expression of TNIP2 gene on AP and AP-induced myocardial injury. MATERIAL AND METHODS To investigate the effect of TNIP2 on AP and AP-induced myocardial injury, we established an AP cell model and rat model. HE staining was applied for histological examination. ELISA was used to determine the level of pro-inflammatory cytokines (TNF-α and IL-6) and myocardial injury markers (LDH and CK-MB). QRT-PCR and Western blot analysis were performed to determine the mRNA and protein level of related genes, respectively. RESULTS We found that the protein level of TNIP2 was relatively higher in the normal AR42J cells. At 4 h after stimulating with cerulein, the protein level of TNIP2 decreased, reached a minimum at 8 h, and then gradually increased. We also found that TNIP2 was correlated with the activation of NF-κB in cerulein-stimulated AR42J cells, and TNIP2 over-expression inhibited the inflammatory response caused by cerulein. Moreover, our results suggest that TNIP2 over-expression relieved the cerulein-triggered inflammatory response and AP-induced myocardial injury in mice. CONCLUSIONS TNIP2 was shown to exert a protective effect on AP and AP-induced myocardial injury.

[Serum levels and clinical significance of high mobility group protein B1 in patients with delayed encephalopathy after acute carbon monoxide poisoning].

OBJECTIVE: To investigate the changes in serum level of high mobility group protein B1 (HMGB1) in patients with delayed encephalopathy after acute carbon monoxide poisoning and the clinical significance of these changes. METHODS: Thirty-four patients with delayed encephalopathy after acute carbon monoxide poisoning (delayed encephalopathy group), 30 normal controls (control group), and 32 cases of acute carbon monoxide poisoning without delayed encephalopathy (carbon monoxide poisoning group) were recruited in this study. The serum HMGB1 level was determined by enzyme-linked immunosorbent assay. The correlation between serum HMGB1 level and scores of the activity of daily living scale (ADL), Information-Memory-Concentration Test (IMCT), and Hasegawa dementia scale (HDS) was determined. RESULTS: In the acute stage of carbon monoxide poisoning, the serum HMGB1 level of delayed encephalopathy group was significantly higher than those of the carbon monoxide poisoning group and the control group (P < 0.01). In the delayed encephalopathy group, serum HMGB1 level in the convalescent stage was significantly lower than that in the acute stage (P < 0.05); ADL score was higher and HDS and IMCT scores were lower in the acute stage than in the convalescent stage (P < 0.01). In the delayed encephalopathy group, serum HMGB1 level was positively correlated with HDS and ADL scores in both acute stage and convalescent stage (correlation coefficients: 0.612, 0.607, 0.609, and 0.612, P < 0.01). CONCLUSION: HMGB1, as an important late mediator of inflammation, is involved in the inflammatory reaction in delayed encephalopathy, and is positively correlated with HDS and ADL scores, indicating that it can be used as one of the major indicators in monitoring carbon monoxide poisoning.