Objective To investigate the clinical significance and the content of soluble P selection in the patients with ischemic cerebrovascular disease(ICVD)Methods Using the means of an enzyme linked immunosorbent assay,the contents of soluble P selectin (sP selection) were measured in 28 patients with ICVD,45 patients with stroke and 33 health persons.We observed its content changes form atherosclerosis to different stages of ICVD,and the effect of M ASA.Results sP selection in different stages of ICVD group was higher than in the patients with atherosclerosis( P

Objective To research early diagnosis and treatment of acute spontaneous spinal epidural hematoma (SSEH). Methods Medical records of 13 SSEH patients adimtted in Timone Ste Marguerite Hospital,France and Ruijin Hospital,China from 1985 to 2000 were retrospectively reviewed.The etiology, neurological symptoms, neuroradiology therapy, as well as the prognosis of this rare disease are discussed in comparison with the literaturs.Results Six of thirteen SSEH wee relatd with innormal coagulation. All patients had the same original symptom which was radicular pain. Eleven cases were diagnosed by MRI. After decompressive surgery, recovery occurred in 3 of 5 patients. Five of 8 patients had a favorable outcome after medical treatment. Conclusions The majority of spontaneous hematomas results from a rupture of the venous plexus. It could be diagnosed according typical symptoms and MRI. Decompressive surgery is urgent but not unique. A idiosyncratic type which has a spontaneous complete recovery could be found.

Objective To investigate the effect of resveratrol on murine macrophage cell line (RAW264 .7 cells) polarizing phenotype induced by lipopolysaccharide .Methods RAW264 .7 mouse macrophages seeded in a 6 well plate ,then randomly divided into phosphate buffer saline(PBS) control group ,LPS (100 ng/mL) group ,and LPS (100 ng/mL)+ resveratrol (30 μmol/L) group .In the LPS+ resveratrol group ,LPS was added after incubation with resveratrol for 12 h .Cells were harvested and superna‐tant were collected after incubation with LPS for 12 h .Both the mRNA expression levels of M1 associated markers iNOS and TNF‐αand M2 associated markers IL‐10 ,PPARγ and Arg‐1 were measured by real time quantitative PCR .Expression of iNOS ,Arg‐1 protein were detected by Western blot ,inflammatory factor IL‐12 p40 ,IL‐10 and TNF‐αprotein in the supernatant of were assayed by ELISA .Results PCR detection showed that the mRNA expression levels of M1 associated markers iNOS and TNF‐αin the LPS group were significantly higher than that of LPS+ resveratrol group(P<0 .05) ,but the mRNA expression levels of M2 associated markers IL‐10 ,PPARγand Arg‐1 were significantly lower than that of LPS+ resveratrol group(P<0 .05) .Compared with LPS+resveratrol group ,western blot assay showed that iNOS protein level in LPS group was significantly higher than it (P<0 .05) ,but Arg‐1 protein level was significantly lower than it(P<0 .05) .The levels of IL‐12 p40 and TNF‐αin LPS group were significantly higher than that in LPS+ resveratrol group(P<0 .05) ,but the levels of IL‐10 was significantly lower than it(P<0 .05) .Conclusion Resveratrol may promote LPS stimulated RAW264 .7 macrophage polarization to M2 phenotype .

Objective To research the mechanism of High Volume Hemofiltration (HVHF) on acute lung injury (ALI) induced by LPS in dogs. Methods After injection of LPS (650 ?g/kg) via central vein within 30 min, Sixteen healthy hybrid male dogs were divided into control group and treatment group randomly (n=8). PaO2、PaCO2 in artery blood were recorded. Contents of TNF-?、IL-6 and IL-10 in plasm were measured by radioimmunity. The activity of NF-?B in lung homogenate was measured by flow cytometer. The content of surfactant protein B (SP-B) in lung homogenate was measured by Western-blotting.Changes of lung histopathology was observed via electron microscopy. Results After injection of LPS, PaO2 and PaO2/FiO2 began to decrease. PaO2 and PaO2/FiO2 in treatment group kept higher than that in control group (P

Objective To discuss the effects of proteinase-activated receptor-2( PAR-2 )agonists on intestinal SIgA levels in rats with severe acute necrotizing pancreatitis( SAP). Methods This study established SAP rat model and observed the levels of TNF-α and IL-6 in intestinal mucosa,SIgA content in intestinal mucus and histopathological changes of intestinal mucosa 6,12,and 24 h after establishment of model. The univariate analysis was used to compare the difference among groups. Linear correlation analysis was used to compare correlation between inflammatory mediators( TNF-α,IL-6 )and SIgA content in intestinal mucus,as well as the histopathological scores of intestinal mucosa. Results The level of TNF-α and IL-6 in intestinal mucosa and histopathological scores of intestinal mucosa were all significantly increased but SIgA content was decreased in model group at each time point after establishment of model,as compared with the sham-operated group(P﹤0. 05). The level of TNF-α and IL-6 in intestinal mucosa and histopathological scores of intestinal mucosa were all significantly decreased while SIgA content in intestinal mucus increased in pretreatment group at each time point after establishment of model,as compared with the model group(P﹤0. 05). There was a positive relationship between inflammatory mediators(TNF-α,IL-6)in intestinal mucosa and histopathological scores of intestinal mucosa(P﹤0. 01). There was a negative relationship between inflammatory mediators(TNF-α,IL-6)and SIgA content in intestinal mucus(P﹤0. 05). Conclusion Intestinal mucosa immune barrier was impaired in the early stage of SAP in rats. PAR-2 agonist has therapeutic effects on intestinal mucosa immune barrier,which is related to the inhibition of excessive release of inflammatory mediators( TNF-α and IL-6)in rats with SAP.

Objective To evaluate the efficacy of early continuous high-volume-hemofiltration in the treatment of patients with severe acute pancreatitis (SAP).Methods Based on the method of prospective,randomized and controlled clinical trial,60 patients with SAP between January 2005 and July 2011 from the First Affiliated Hospital of Nanchang University were divided into control group and hemofiltration group.The hemofiltration group was treated with early continuous high-volume-hemofiltration and not in the control group.The changes of vital signs,clinical symptoms and laboratory indicators were compared between the two groups before and after the treatment.Results After hemofiltration,the clinical symptoms such as abdominal pain,fever,tachycardia and respiratory distress in hemofiltration group were significantly remitted compared to those in the control group (P ＜0.05).The APACHE Ⅱ score (13.3 ± 1.0 vs 14.1 ± 1.2) and the level of TBil[(20.4±11.3) μmol/L vs (28.1 ±10.9) μmol/L],creatinine[(178.7 ±71.8)μmol/L vs (215.6 ± 51.3) μmol/L],blood urea nitrogen[(10.1 ± 5.6) mmol/L vs (13.2 ± 3.8) mmol/L] and ALT[(51.3 ± 13.2) U/L vs (62.5 ±14.3) U/L] were decreased compared to those in the control group (all P values ＜0.05).The level of PaO2/FiO2(197.3 ±32.4 vs 178.3 ±31.7) was increased (P ＜ 0.05).After hemofiltration,heart rate was decreased gradually (P ＜ 0.05) in the hemofiltration group than in the control group.Mean artery pressure (mAP) increased gradually (P ＜ 0.05) in the hemofiltration group than in the control group.Conclusion Early continuous high-volume-hemofiltration has significant effects on the treatment of SAP including the improvement of clinic symptoms,the blockade of development from systemic inflammatory response syndrome (SIRS) to multiple organ dysfuction syndrome(MODS),improvement of organ function and prevention from the complications.It may become one of the important therapies for SAP.

Objective To explore the mechanism and effect of miR-146a on alveolar macrophages and to observe the changes of miR-146a expression in the LPS-induced alveolar macrophages. Method NR8383 alveolar macrophages were divided into LPS-stimulated group and control group, and the cells of former group were treated with LPS ( 1 μg/mL) and then incubated for 3 h, 6 h and 12 h, respectively. The level of TNF-α in the supernatant of cells was assayed by using enzyme-linked immunosorbent assay (ELISA), and the expression of miR-146a of cells was detected by using Real-Time PCR (TaqMan probe).Statistical analysis carried out by using SPSS 13.0 software package in which One-way ANOVA and Student's t-test were used. Results Compared with control group, the levels of TNF-α in the supernatant of cells were significantly increased 3 h, 6 h and 12 h after LPS challenge (P ＜ 0.01 ). The expression of miR-146a increased 6 h and 12 h after LPS stimulation in NR8383 cells( P ＜0.01 ), and it had an upward tendency.Conclusions The expression of miR-146a in alveolar macrophages increases after LPS-stimulation. It hints miR-146a may be involved in the regulation of the inflammatory responses produced by alveolar macrophages.

ObjectiveTo observe the effect of acetylcholine (ACh) on lipopolysaccharide (LPS) induced inflammatory model of rat alveolar macrophages, and to observe the effect of the acetylcholinesterase inhibitor physostigmine (Phy) on the anti-inflammatory effect of ACh.Methods The rat alveolar macrophages NR8383 were cultured in vitro, which were divided into five groups: blank control group, LPS group (stimulated with 1 mg/L LPS for 12 hours), LPS+ ACh group (0.01, 0.1, 1, 10, 100μmol/L of ACh were added for 5 minutes before LPS stimulation), LPS+ Phy group (1 mmol/L Phy was added for 5 minutes before LPS stimulation), and LPS+ ACh+ Phy group (1 mmol/L Phy and 10μmol/L ACh were added for 5 minutes before LPS stimulation). The supernatants were collected in each group, the enzyme-linked immunosorbent assay (ELISA) was used to assay the contents of tumor necrosis factor-α (TNF-α), interleukins (IL-1β, and IL-6). The activity of acetylcholine esterase (AChE ) in the supernatant was also determined.Results① The contents of TNF-α (ng/L: 605.09±57.13 vs. 34.07±8.62), IL-1β (ng/L: 377.09±28.55 vs. 32.33±10.62) and IL-6 (ng/L: 558.04±77.45 vs. 42.62±11.21) in the LPS group were significantly higher than those in the blank control group (allP< 0.05). These results indicated that the inflammatory model of rat alveolar macrophages was constructed successfully.② ACh with the final concentrations of 0.01, 0.1, and 1μmol/L had less influence on the production of TNF-α, IL-1β and IL-6 in the culture supernatants of alveolar macrophages stimulated with LPS compared with LPS group (allP> 0.05). Nevertheless, 10μmol/L and 100μmol/L ACh notably reduced the production of TNF-α (ng/L: 451.19±30.67, 332.19±32.19 vs. 604.96±22.56), IL-1β(ng/L: 261.08±24.78, 143.98±28.39 vs. 367.06±10.44) and IL-6 (ng/L: 342.75±54.60, 235.48±29.75 vs. 562.69±63.34) in the culture supernatants compared with the LPS group (allP< 0.05).③ The activity of AChE in the LPS group was significantly higher than that in the blank control group (kU/L: 5.21±0.63 vs. 3.09±0.10,P< 0.05). The activity of AChE was successfully inhibited by 1 mmol/L acetylcholinesterase inhibitor Phy pretreatment compared with that in the LPS group (1.51±0.12 vs. 5.21±0.63,P< 0.05).④ The level of TNF-α (ng/L: 183.17±35.44 vs. 451.19±30.67), IL-1β (ng/L: 91.49±12.27 vs. 261.08±24.78) and IL-6 (ng/L: 108.17±22.82 vs. 342.75±54.60) in the culture supernatants of LPS+ ACh+ Phy group was significantly decreased as compared with LPS+ ACh group (allP< 0.05).Conclusions ACh with the final concentrations of 10μmol/L and 100μmol/L can inhibit the LPS induced inflammatory reaction in alveolar macrophages. The acetylcholinesterase inhibitor Phy can reinforce the ACh-mediated anti-inflammatory effect on alveolar macrophages inflammatory model.

ObjectiveTo investigate the protective effect of transfected microRNA-146a (miR-146a) on mice with sepsis-induced acute lung injury (ALI) in vivo.Methods Twenty-four healthy male BALB/C mice were randomly divided into sham group, sepsis group, transfection group and transfection control group, eachn = 6. Mice in transfection group were given miR-146a agomir loaded by in vivo-jetPEITM via airway before reproduction of model, and mice in transfection control group were given negative control loaded by in vivo-jetPEITM only via airway. The septic model was reproduced by cecal ligation and puncture (CLP) 12 hours after transfection , and the mice in the sham group underwent laparotomy and closure only without ligation and puncture of the cecum. The mice of each group were sacrificed at 24 hours post-operation. The expression of miR-146a in lung tissue was determined by real time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and the quantity of tumor necrosis factor-α (TNF-α) in the bronchial alveolar lavage fluid (BALF) was determined with enzyme-linked immunosorbent assay (ELISA). The wet/dry ratio of lung (W/D) was determined. The pathohistological changes in the lung were observed and scored. Results The expression of miR-146a showed a significant increase in sepsis group, transfection group and transfection control group, which were (3.56±0.43), (27.64±3.46) and (3.72±0.54) folds of that in sham group, respectively (P< 0.05 orP< 0.01). The miR-146a expression in transfection group was significantly increased compared with sepsis group and transfection control group (bothP< 0.01), but no statistical difference in the expression was found between sepsis group and transfection control group (P> 0.05). Compared with the sham group, higher level of TNF-αin the BALF was found in the sepsis group, transfection group and transfection control group (ng/L: 511.65±43.47, 305.74±34.76, 492.27±42.21 vs. 50.72±7.23, allP< 0.01). The level of TNF-α in transfection group was significantly lower than that in sepsis group and transfection control group (bothP< 0.01). Compared with the sham group, the W/D ratio of lung in sepsis group, transfection group and transfection control group showed a significant increase (6.11±0.32, 5.02±0.29, 6.05±0.43 vs. 4.18±0.10, allP< 0.01). The W/D ratio of lung in transfection group was significantly lower than that of sepsis group and transfection control group (bothP< 0.01). The lung injury score of transfection group was significantly lower than that of sepsis group and transfection control group (6.12±0.75 vs. 10.53±1.52, 9.73±1.08, bothP< 0.01).Conclusions miR-146a agomir loaded by in vivo-jetPEITM instillation into airway was able to increase the expression of miR-146a in the lung tissue of septic mice. Up-regulation of miR-146a inhibit the release of the inflammatory cytokine TNF-α stimulated by sepsis, and alleviate inflammatory reaction and lung tissue injury in mice with sepsis-induced ALI.

[ ABSTRACT] AIM:To study the effect of idazoxan ( IDA) on the permeability of blood-brain barrier ( BBB) and the expression of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) in mouse ex-perimental autoimmune encephalomyelitis (EAE).METHODS: Female C57BL/6 mice (n=36) were randomly divided into control group, EAE group and IDA group, with 12 mice in each group.EAE was induced by myelin oligodendrocyte glycoprotein 35-55 ( MOG35-55 ) .IDA (2 mg/kg, ip, bid) was administered for 15 d after immunization.The neurological defects of the mice were observed daily and scored.The pathological changes were observed under microscope with HE stai-ning and LFB myelin staining.The BBB permeability was detected by Evans blue extravasation.The expression of MMP-9 and TIMP-1 in the brain of EAE mice was determined by Western blotting.RESULTS: Compared with EAE group, the score of neurological defects in IDA group was decreased, the inflammation was relieved, the BBB permeability was re-duced, and the expression MMP-9 and the ratio of MMP-9/TIMP-1 were decreased ( P<0.05 ) .CONCLUSION: The neuroprotective effect of IDA on mouse EAE might be related to the down-regulation of MMP-9 and the ratio of MMP-9/TIMP-1, thus reducing the degradation of BBB and the permeability of BBB, and ameliorating the pathologic process of EAE.