ObjectiveTo investigate the expressions of IL-10,tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in serum and lung tissue of COPD rats in order to elucidate the potential mechanism of airway inflammation. MethodsForty-five healthy adult male SD rats were randomly divided into a COPD model group (n=30) and a normal control group (n=15). The COPD rat model was established by intratracheal instillation of lipopolysaccharide (LPS) and exposure to cigarette smoke for 28 days. The concentrations of IL-10,TNF-α and IFN-γ in serum and lung tissue were measured by ELISA. ResultsTNF-α level of serum and lung tissue in the COPD model group increased significantly compared with the control group(P<0.05),while the levels of IFN-γ and IL-10 decreased significantly[serum:(44.68±8.67) ng/L vs. (75.96±10.59) ng/L;lung tissue:(64.55±9.03) ng/L vs. (94.06±8.71) ng/L,P<0.01]. The level of IL-10 in serum and lung tissue was negatively correlated with TNF-α (serum:r=-0.67,lung tissue:r=-0.80,P<0.01). The level of IL-10 in serum and lung tissue was positively correlated with IFN-γ (serum:r=0.64,lung tissue:r=0.72,P<0.01). The level of IL-10 in serum and lung tissue was negatively correlated with the percentage of neutrophils(serum:r=-0.70,lung tissue:r=-0.67,P<0.01). ConclusionIn COPD rats,down regulation of IL-10 plays an important role in regulation of airway inflammation.
Objective To study the effect of Fe 3+ -modified carborymethyl celluiose (Fe 3+ -CMC ) on preventing postoperative adhesion and inhibiting the expressions of tumor necrosis factor-α (TNF-α) and fibroblast growth factor (FGF) in the injured parts of postoperative peritoneum. Methods Fourty Wistar mice were divided into 2 groups randomly, and abdominal adhesion models were made, then 0.9% NaCl (control group) and Fe 3+ -CMC (experimental group) were sprayed into the wound surface of abdominal cavity. All mice were killed to observe the adhesion condition on day 14 after operation. Another 120 Wistar mice were divided into 2 groups randomly, and abdominal adhesion models were made as mentioned above. Ten mice were killed which were chosen randomly from 2 groups on day 1, 3, 5, 7, 14 and 60, respectively. The expressions of TNF-α and FGF in the peritoneal injured and adhesion tissues were observed by immunohistochemistry technique. Results The adhesion grade in experimental group was much lower than that in control group ( P ＜ 0.01). The expression of TNF-α (day 3-7 after operation) and FGF (day 5-7 after operation) in experimental group were lower than those in control group ( P ＜ 0.05).Conclusion Fe 3+ -CMC can decrease postoperative adhesion grade and prevent the expressions of TNF-α and FGF in injured parts of postoperative peritoneum.
Objective To investigate influence of genders on the activity of nuclear factor-kappa B (NF-κB) in lungs of endotoxemic rats. Methods Twenty female and 20 male Wistar rats were randomly divided into four groups as follow: female control group (n=10), male control group (n=10), male endotoxemic group (n=10), and female endotoxemic group (n=10). The endotoxemic rats model was made by injecting lipopolysaccharide (5 mg/kg) into the abdominal cavity. Tissue samples were collected from the lungs in different groups and electrophoresis mobility shift assay was used to measure the activity of NF-κB. The levels of serum TNF-α and estrogen were measured at the same time. Results There was no significant difference between the activities of NF-κB in male and female control groups (1.33±0.24 vs 1.47±0.40）, and there was also no significant difference between other items in these groups as well (Pgt;0.05). Yet, the activity of NF-κB (female: 12.10±2.89; male: 19.53±2.12) and the level of TNF-α 〔female: (4.10±0.72) ng/ml; male: (6.37±1.29) ng/ml〕 were significantly increased after injection of lipopolysaccharide (Plt;0.01), and the indices in female group were significantly lower than those in male group (Plt;0.01). Correlation analysis showed that there was a positive relation between the activity of NF-κB in lungs and the level of TNF-α (female: r=0.921 1, P=0.013; male: r=0.907 2, P=0.017), and there was a negative correlation between the activity of NF-κB and the level of estrogen (female: r=-0.887 5, P=0.017; male: r=0.872 3, P=0.022) in both male endotoxemic group and female endotoxemic group (Plt;0.05). Conclusion Gender may be one of the factors that influence the activity of NF-κB in the lungs of endotoxemic rats. While on the other hand, endogenous estrogen may protect the lungs of endotoxemic rats from injury by inhibiting the activity of NF-κB.
【Abstract】ObjectiveTo explore the effects of p38 mitogenactivated protein kinase (MAPK) on apoptosis of small intestinal epithelial cells after transplantation in rats. MethodsSmall intestinal transplantation was performed in SD and Wistar rats. The recipients were divided into three groups: isograft group (Wistar→Wistar group), allograft group (SD→Wistar group) and allograft+cyclosporine A group (SD→Wistar+CsA group). The grafts were harvested on day 1, 3, 5 and 7 after operation. All graft samples were subjected to histological examination. The apoptosis of graft epithelial cells was detected by TUNEL method. p38 MAPK was measured by Westernblotting method and serum TNFα was determined by ELISA. ResultsMild, moderate and severe rejection reaction occurred in the SD→Wistar group, it was showed that the number of apoptotic cells increased with the severity of the rejection reaction by TUNEL. In SD→Wistar group, the numbers of apoptotic cells were significantly higher than those of the other two groups （P＜0.01）. The severity of rejection reaction in SD→Wistar+CsA group was less than that of SD→Wistar group and the number of apoptotic cells increased with the severity of the rejection reaction (P＜0.01). The level of serum TNFα varied with the apoptotic degree of small intestinal epithelial cells in SD→Wistar group and SD→Wistar+CsA group （P＜0.01）. The expression of p38 MAPK increased with the number of the apoptotic cells in SD→Wistar group and SD→Wistar+CsA group （P＜0.01）, but there was no evident change in Wistar→Wistar group （Pgt;0.05）. The expression of p38 MAPK and the level of serum TNFα were positively correlated with apoptosis in small intestinal rejection after transplantation （r=0.875， P＜0.01； r=0.837， P＜0.01）. p38 MAPK and TNFα were also positively correlated （r=0.826，P＜0.01）. ConclusionApoptosis plays an important role in small intestinal rejection. p38 MAPK is involved in apoptosis and is an important regulator in signal pathway of cell apoptosis.
【Abstract】ObjectiveTo explore the effect of glutamine on immune function of rat with obstructive jaundice and its possible mechanism. MethodsFifty male Wistar rats were randomly divided into three groups: Control group (n=10)， obstructive jaundice group (n=20) and glutamine treatment group (n=20). The serum concentration of TNF-α, IL-10 was detected by using radioimmune method. Liver function was measured through automated biochemistry analyzer. The animal model of obstructive jaundice was established by ligating the rat’s common bile duct. Bacteria cultures were performed with the rat’s tissues of lung, spleen, liver and kidney respectively. ResultsCompared with control group, obstructive jaundice group showed statistically lower serum level of TNF-α, and statistically higher serum level of IL-10, TBIL, ALT and AST during the first and the second week after ligation of common bile duct. During the first and second week after administration of glutamine, the serum TNF-α of glutamine treatment group was statistically higher than that in control group and obstructive jaundice group. Meanwhile, glutamine treatment group showed statistically lower serum level of IL-10, TBIL, ALT and AST than obstructive jaundice group. There were statistically less bacteria translocations in glutamine treatment group than those in obstructive jaundice group. Conclusion Glutamine can increase the immune function by changing serum concentration of TNF-α, IL-10 and decrease the bacteria translocation.
【Abstract】Objective To study the influence of early hemofiltration on plasma concentrations of proinflammatory cytokines TNF-α and IL-1β and their transcription levels in severe acute pancreatitis (SAP) pigs. Methods The model of SAP was induced by retrograde injection of artificial bile into pancreatic duct in pigs. Animals were divided randomly into two groups: SAP hemofiltration treatment group (HF group, n=8) and SAP no hemofiltration treatment group (NHF group, n=8). TNF-α and IL-1β plasma concentrations were measured by ELISA. Their transcription levels in the tissues of pancreas, liver and lung were assayed by semi-quantitative reverse transcription polymerase chain reaction. Results After hemofiltration treatment, the plasma concentrations of TNF-α and IL-1β increased gradually but were lower than those of NHF group at the same time spot 〔at 6 h after hemofiltration treatment, (618±276) pg/ml vs (1 375±334) pg/ml and (445±141) pg/ml vs (965±265) pg/ml, P＜0.01〕. At 6 h after hemofiltration treatment, the transcription levels of TNF-α and IL-1β in tissues of pancreas, liver and lung were lower than in NHF group (57.8±8.9 vs 85.7±17.4, 48.0±8.1 vs 78.1±10.2, 46.2±9.6 vs 82.4±10.5; 55.9±9.0 vs 82.2±15.7, 40.6±9.2 vs 60.0±10.6, 35.7±9.8 vs 58.1±9.3, P＜0.01). Conclusion Early hemofiltration can reduce TNF-α and IL-1β plasma concentrations and transcription levels in SAP pigs.
Objective To investigate the changes and significance of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-α (TNF-α) in intestinal mucosa in rats with obstructive jaundice. MethodsTwenty-four SD rats were randomly divided into sham operation (SO) group and bile duct ligation (BDL) group, and each group were randomly divided into the day 7 and day 14 subgroup. The expression of ICAM-1 was assayed by immunohistochemistry. The level of TNF-α was determined by ELISA. The activity of myeloperoxidase (MPO) and diamine oxidase (DAO) was determined as well.ResultsOn the day 7 and 14, in the bile duct ligation group, the ICAM-1 protein was mainly expressed in the intestinal epithelia and increased with the time on (P＜0.05); the level of TNFα increased from （14.25±1.01） ng/g to （23.83±1.43） ng/g （P＜0.01）； the intestinal DAO activity decreased from （1.70±0.36） U/mg to （1.22±0.41） U/mg （P＜0.01），and plasma DAO activity increased from （6.44±1.74）U/ml to （8.93±1.29） U/ml （P＜0.01）; the MPO activity increased from （2.85±1.22 ） U/mg to （4.93±1.37） U/mg （P＜0.01）. ConclusionThe ICAM-1 expression is significantly upregulated and the level of TNFα significantly increases after bile duct ligation, which may be involved in the PMNmediated injury to intestinal mucosa.
【Abstract】Objective To explore the dynamic expression of TNF-α and VEGF in the development of esophageal varices in rats with portal hypertension. Methods Sixty male SD rats were randomly divided into the experimental group and the control group. In the experimental group, a two-stage ligation of portal vein plus ligation of the left adrenal vein was performed.After establishment of the model, the expression of TNF-α、VEGF and PCNA in the lower esophagus was detected with immunohistochemical SP technique on 7 d、14 d、21 d and comparision of these data with control group was performed respectively. In the control group, a sham-operation was performed, was also divided.Results The portal venous pressure in the experimental group was significantly higher than that of the control, so did the vessel number and the total vascular area of the submucosal veins in the lower esophagus. Compared with the control subgroups, the expression of TNF-α and VEGF on the 21 d subgroup was ber, while PCNA was ber on the 14 d and 21 d. Conclusion In the development of esophageal varices of portal hypertension, VEGF possibly plays a role in the varices developemt, and TNF-α may be responsible for the damage of esophageal mucosa.
ObjectiveTo investigate the protective mechanism of prostaglandin E1 against hepatic ischemia reperfusion injury.MethodsUsing 45minute ischemiareperfusion rat model in normal temperature, PGE1 was injected into portal vein before ischemia. An hour later blood was taken from portal vein to examine the enzyme levels, including GOT, GPT, LDH and TNFα, ET1. The alteration of pathological morphology of the ischemia lobe was observed.ResultsThe three enzemes, TNFα, ET1 levels of ischemiareperfusion group were significantly higher than those of the control group (P＜0.01). The indices of the PGE1 group were much lower than those of the ischemiareperfusion group (P＜0.01), but little higher than those of the control group (P＞0.05). The control group had obvious alteration in pathological morphology, but only slight alteration in PGE1 group, compared with the control group. ConclusionPGE1 protects against ischemiareperfusion injury of the liver.
Objective To study the change in serum levels of soluble CD14, tumor necrosis factor-α, E-selectin, interleukin-10 and mean arterial pressure, as well as their relationship to infection during the pathophysiologic process in endotoxemia of rabbits. Methods Sixteen rabbits were randomly divided into two groups: group A, as a control group; group B, endotoxemia group. The model of rabbit with endotoxemia were used. Endotoxin at a dose of 1.5 mg/(kg·h) or 3 mg/(kg·h) was continuously infused through external jugular vein within 2 hours, 1 hour respectively. The change of levels of serum soluble CD14, tumor necrosis factor-α, interleukin-10 and E-selectin were observed at 0 (time before infusion of endotoxin), 30, 60, 120, 180, 240, 300 minutes, while mean arterial pressure was measured by polygraphy system. Results In the group B,there was an increase of content of soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin following 30, 120 minutes respectively,and mean arterial pressure was lower than that of group A at same time points. Conclusion The results suggest that soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin may play an important role during the change of infection and that these changes may be closely related with severe infection.