Objective To observe the serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), platelet 5-HT and blood platelet count, emotion and burn injury healing of patients with moderate and severe burn injury and anxiety-depression symptoms. Methods In-patients with moderate and severe burn injury were selected from 2003.4 to 2005.2 and then divided into anxiety-depression group and control group according to their anxiety-depression scores by Hamilton Rating Scale for Depression (HAMD ) and Hamilton Rating Scale for Anxiety (HAMA) 3 days after being burnt. Routine therapy was given to two groups, which lasted 1 month. Their scores of anxiety and depression and the degree of injury healing were observed, and the serum levels of TNF-α and IL-6, platelet 5-HT and blood platelet count were measured in the two groups. Results Fifty-one in-patients with moderate and severe burn injury were divided into the anxiety-depression group (24 cases) and the control group (27 cases). After 30-day treatment, the depression scores did not decrease in the anxiety-depression group (P=0.12), but the anxiety scores decreased (P=0.00). In the anxiety-depression group, the burn injury healing time was postponed (P=0.00), the serum levels of TNF-α increased (P=0.00), and the platelet 5-HT levels decreased (P=0.04) before and after treatment. Conclusion Depressive reaction occurs in patients with moderate and severe burn injury, which is a continuously negative emotion. It can lead to high levels of serum TNF-α, reduction in platelet 5-HT, and delayed burn injury healing time. Due to the limited sample size and different location of patients, there may be some bias in this conclusion. We are prepared to increase the sample size and select patients in the same region in further relevant studies.
Objective To study the effect of tumor necrosis factor-α( TNF-α) onhypermetabolism of skeletal muscle protein in rats with chronic obstructive pulmonary disease ( COPD) and explore its underlying mechanism. Methods Forty-five SD rats were randomly divided into a normal control group, a COPD group and a COPD + TNF-α group, with 15 rats in each group. COPD model was established by passive cigarette smoking in COPD group and COPD + TNF-αgroup. Then the extensor digitorium longus muscles ( EDL) were dissected and incubated in vitro muscle incubation system with adequate oxygen supply. The EDL were either cultured with or without recombinant rat TNF-α( 10 μg/L) . The mRNA and protein expressions of proteasome subunit C2 in EDL were quantified by real-time quantitative PCR and Western blot analysis, respectively. Results The mRNA and protein expressions of proteasome subunit C2 were both significant higher in the COPD group and COPD + TNF-αgroup than those in the normal control group( P lt;0. 01 or 0. 05) . The COPD+TNF-αgroup had higher expression of proteasome subunit C2 mRNA than that in the COPD group( P lt; 0. 01) , whereas the protein expression was not significantly different( P gt; 0. 05) . Conclusion Incresed proteolytic metabolism in skeletal muscle in COPD might be regulated by TNF-αactivated ubiquitin-dependent pathway.
Objective To summarize the change in the cytokine network, the classification of various cytokines, interaction, and systemic impact on patients with acute pancreatitis (AP). Methods The recently published literatures in domestic and abroad about advancement of cytokines in AP were reviewed. Results Cytokines had a complex network and interactions. There were a variety of regulatory mechanisms. The tumor necrosis factor-α (TNF-α) and interleukin cytokines played important roles in the progress of AP. Conclusions Change of cytokines during AP is a complex process. Any separate regulation for the release of sigle factor has no significant effect on the disease. The treatment according to immune balance should be a better direction.
Objective To investigate the effects of methylprednisolone on airway inflammation of chronic bronchitis in rats, and to explore its possible mechanism. Methods Forty SD rats were randomly divided into five groups, ie. a blank control group, amethylprednisolone control group, a model group, and two methylprednisolone intervention groups. Chronic bronchitis model was established by cigarette inhalation in the model group and two intervention groups. Methylprednisolone was injected intraperitoneally in the two intervention groups before exposing to cigarette smog ( at the dose of 1 mg/ kg and 10 mg/ kg, qd,respectively) . The protein expression of phosphodiesterase 4D ( PDE4D ) in trachea and lung samples was determined by immunohistochemical staining. The average optical density of positive staining of PDE4D was determined by image analysis technique and gray scale scanning. Bronchoalveolar lavage fluid ( BALF) was collected for total and differential cell counts, and the concentrations of TNF-αand interleukin-8 ( IL-8) in BALF were detected by ELISA. Results Cigarette smoking induced obvious airway inflammation in themodel group, and the inflammation was alleviated in the two methylprednisolone intervention groups.Compared with the two control groups, the expression of PDE4D was obviously elevated in tracheal and lungs in the model group( P lt; 0. 05) . Moreover, the increased expression of PDE4D was positively related with theincreased release of TNF-αand IL-8 in BALF. The expression of PDE4D and the release of TNF-αand IL-8 in BALF were decreased after the treatment with methylprednisolone in a dose-dependent manner ( P lt;0. 05) . Compare with the low dose intervention group, there was no markedly difference related to PMNnumber and TNF-α release in the high dose intervention group ( P gt; 0.05) . Conclusions Methylprednisolone may alleviate airway inflammation of chronic bronchitis by inhibiting the expression of PDE4D in rats. Inhibition of PDE4D may down-regulate TNF-αactivity, which may further reduce IL-8 release and alleviate airway inflammation.
ObjectiveTo explore the mechanism of liver capillary permeability in rats with severe acute pancreatitis (SAP). MethodsTotally 40 healthy Sprague-Dawley (SD) rats were randomly divided into two groups: sham operation (SO) group and SAP group, SAP group were divided into four subgroups according to sampling time (3 h， 6 h, 12 h， and 24 h). The model was established by injecting 5% sodium taurocholate retrogradely into pancreaticobiliary ducts. The changes of tumor necrosis factor-α (TNF-α), pathohistology, and tissue moisture content were compared among different groups. Liver occludin protein expression was analyzed by immunohistochemistry method, and occludin mRNA was measured by RT-PCR. ResultsThere was no significant pathological changes of liver tissue in the SO group. Typical pathological changes of SAP， such as interstitial edema, vasodilatation, infiltration of inflammatory cells, were found in the SAP group. TNF-α level and tissue moisture content of each phase increased gradually, and the highest level appeared at 24 h within the observing period. The two above indicators at different time point in subgroups were significantly different from each other and higher than those in the SO group (Plt;0.05)． In the SAP group, the expression of occludin and it’s mRNA began to decrease at 3 h to the bottom at 6 h and rebounced significantly at 12 h, 24 h compared with those at 6 h (Plt;0.05), but still lower than those in the SO group (Plt;0.05). ConclusionUpregulation in TNF-α and subsequent downregulation in occludin protein and mRNA maybe bly related to the severe liver capillary permeability in rats with SAP.
【Abstract】ObjectiveTo investigate the effect of Salvia Miltiorrhiza (SM) and Shengmai injection （SI） in treating systemic inflammatory response syndrome (SIRS) and their mechanism. Methods The animal model of SIRS was established by injectinglipopolysaccharide(LPS, 1 mg/kg)intraperitoneally. Forty Wistar rats were randomly divided into four groups: control group, SM group, SI group and combined treatment group (SM+SI group), which were treated with normal saline（5 ml/kg） plus LPS（1 mg/kg）, SM（5 ml/kg）plus LPSKG4（1 mg/kg）, SI（5 ml/kg）plus LPS（1 mg/kg）, SM（2.5 ml/kg） plus SI（2.5 ml/kg） and LPS（1 mg/kg） respectively. Six rats of each group were sacrificed for sample collection of blood, liver, lung and kidney 8 hours after LPS injection. Blood routine, serum TNF-α and IL-6 were measured. Specimen of organs were fixed in formalin and sent for routine pathological examination. The survival of other 4 rats of each group were observed untill 48 hours after LPS injection. SPSS 10.0 was used in statistical analysis. Results Two rats in control group died 13 hours and 22 hours after LPS injection respectively, the remaining 2 rats in this group and the rats in other 3 groups survived 48 hours after LPS injection. The white blood cell count of control group was significantly higher than that of other groups. The serum TNF-α and IL-6 of control group were significantly more than those of other groups. Pathological damages were found in all groups, and the most severe ones were in control group. SM and SI could decrease the level of serum TNF-α and IL-6 in the process of LPS-stimulated SIRS, down-regulate the severe inflammatory response, attenuate organ damages of the liver, lung and kidney, and increase forty-eihgt-hour survival rate obviously. Conclusion The experiment provides a theoretical base for clinical use of SM and SI in treatment of SIRS.
Objectve To measure the serum levels of human IL-32 and explore the clincal implication in patients with chronic obstructive pulmonary disease( COPD) at acute exacerbation or stable stage. Methods 120 patients with COPD were recruited, including 60 patients with acute exacerbation COPD and 60 patients with stable COPD from October 2010 to May 2011. Thirty healthy nonsmoking volunteers were included as controls. The concentrations of interleukin-8 ( IL-8) , tumor necrosis factor alpha ( TNF-α) , and IL-32 in serum were measured by enzyme-linked immunosorbent assay ( ELISA) . The correlations among IL-32, IL-8, TNF-αand lung functions were investigated. The datas were analyzed using a statistical software package ( SPSS13. 0) . Variables were compared with one-way ANOVA . The correlations between variables were analyzed using Pearson’s correlation coefficient or Spearman correlation coefficient. Results SerumIL-32 level was significantly higher in AECOPD patients [ ( 174. 56 ±88. 15) ng/L] than that in healthy subjects [ ( 59. 41 ±20. 98) ng/L] and in stable COPD patients [ ( 89. 40 ±33. 84) ng/L]( P lt;0. 05) while serum IL-32 level was also significantly higher in stable COPD patients than in healthy subjects( P lt;0. 05) . The serumIL-32 1evel in patients with acute exacerbation COPD and stable COPD was positively correlated with the serumIL-8 level, TNF-αlevel ( respectively P lt;0. 01) . The serumIL-32 level was negatively correlated with FEV1 /predicted value, FEV1 /FVC and PaO2 ( respectively, P lt;0. 01) . There was no statistical significance of the serum IL-32, IL-8 or TNF-α levels in COPD patients with different severity ( all P gt;0. 05) . Conclusion The serumlevel of IL-32, a newpro-inflammatory cytokine is elevated in COPD patients, which may be involved in the pathogenesis of inflammation in COPD.
Objective To explore the effects of asiaticoside on the activation of nuclear factor kappa B ( NF-κB) and cytokines expression in RAW264. 7 cells induced by lipopolysaccharide ( LPS) . Methods RAW264. 7 cells were allocated to 5 groups, ie. a blank group, a model group stimulated by LPS at dose of 10 μg/mL, and three asiaticoside treatment groups stimulated by LPS and different doses of asiaticoside simultaneously. The effects of asiaticoside ( 10 - 7 , 10 - 6 , 10 - 5 mol /mL) on the proliferation of cells were examined by MTT assay. The activation of NF-κB was detected and analyzed by the laser scanning confocal microscope( LSCM) ,meanwhile the concentrations of TNF-α, IL-1, and IL-10 in supernatants were quantified by ELISA. Results MTT assay showed that asiaticoside ( 10 - 7 , 10 - 6 ,10 - 5 mol /mL) had no effects on the proliferation of RAW264. 7 cells. Asiaticoside significantly decreased the activation of NF-κB, downregulated the secretion of TNF-αand IL-1, and upregulated IL-10 secretion in a dose dependent manner. According to LSCM, the ratio of NF-κB activation was ( 3. 5 ±1. 5) % , ( 75. 7 ±9. 1) % , ( 66. 8 ±7. 1) % , ( 58. 9 ±9. 0) % , and ( 40. 1 ±8. 8) % in the blank, model, and asiaticoside( 10 - 7 , 10 - 6 , 10 - 5 mol /mL) treatment groups respectively. The contents of TNF-α in supernatants were ( 171. 12 ±35. 42, 1775. 45 ±193. 97,1284. 63 ±162. 13,1035. 22 ±187. 97, 598. 90 ±107. 73) pg/mL respectively and IL-1 were ( 5. 66 ±0. 98,26. 93 ±3. 48,22. 41 ±2. 84, 17. 05 ±1. 70, 10. 64 ±1. 29) ng/mL respectively, while IL-10 were ( 25. 23 ±2. 17,71. 75 ±8. 31, 82. 82 ±6. 00, 98. 70 ±8. 84, 119. 97 ±9. 13) pg/mL respectively. Conclusion The antiinflammation mechanism of asiaticoside may be mediated by downregulating inflammatory factors throughNF-κB signal pathway and keeping the balance between proinflammatory and antiinflammatory system.
ObjectiveTo study the effect of bacillus calmette-guerin(BCG) polysaccharides nucleic acid on humoral immunity, interleukin(IL)-8 and tumor necrosis factor(TNF)-αin patients with chronic obstructive pulmonary disease (COPD), and to provide theoretical basis for evaluation of its clinical effectiveness. MethodsThirty hospitalized elderly patients with AECOPD treated from March 2012 to February 2013 and 60 patients with stable COPD treated at the same time were randomly selected as the study subjects. At the same time, 60 healthy people from our physical examination center were also enrolled and divided into two groups:the elderly healthy group (n=30) and nonelderly healthy group (n=30). IL-8, TNF-α, IgA, IgG and IgM levels were determined. The stable COPD group was randomly divided into two groups:group A (n=30) and group B (n=30). Group A received only routine therapy; group B received both routine therapy and intramuscular injection of BCG polysaccharide nucleic acid (0.35 mg/day, three times a week). IL-8, TNF-α, IgA, IgG and IgM levels in peripheral blood were investigated before treatment and one month later. ResultsThere were no statistically significant differences in IL-8 and TNF-αlevels in peripheral blood between elderly healthy group and nonelderly healthy group (P > 0.05), but the IgA, IgG and IgM levels were lower in the nonelderly healthy group than in the elderly healthy group (P < 0.05). Compared with the elderly healthy grouping, IgG and IgM levels were significantly lower in AECOPD group and stable COPD group (P < 0.05), but IL-8 and TNF-αlevels were significantly higher (P > 0.05). There were statistically significant differences in TNF-α, IgA, IgG and IgM levels between group B before and after treatment (P > 0.05). ConclusionsHuman's humoral immunity decreases with age. Elderly COPD patients are at high risks of abnormal immunologic function, particularly in the acute exacerbation period. The BCG polysaccharides nucleic acid can strength patients' humoral immunity. The levels of inflammatory cytokines can be reduced using BCG polysaccharides nucleic acid.
Objective To study the effect and intrinsic mechanism of acute suppurative peritonitis associated ascitic fluid (ASPAAF) on experimental liver injury of rats. Methods Thirty-two male or female Sprague-Dawley (SD) rats were randomly divided into two groups: ASPAAF group (n=16) and control group (n=16), in which 8 ml ASPAAF or normal saline (NS) were injected into the peritoneal cavity, respectively. The rats were killed at each time intervals after peritoneal cavity injection (6 h and 12 h) respectively in two groups and specimens were made to detect the levels of serum TNF-α, endotoxin and liver function (AST, ALT and STB). The level of TNF-α in liver tissues was measured. The pathological change of liver was observed by microscope. Results The levels of TNF-α, endotoxin, ALT, AST and STB in serum and the levels of TNF-α in liver tissues at different time points were markedly higher in ASPAAF group compared with those in control group (P＜0.05), and these indexes increased with increasing time in ASPAAF group (P＜0.05). In ASPAAF group, hepatic tissue appeared hydrops, even spotty necrosis and the changes at 6 h and 12 h were not obvious different. No abnormal pathological change of hepatic tissue was found in control group. Conclusion ASPAAF can induce the injury of the liver in rats, which may involved in TNF-α and endotoxin.