Objective To investigate the relationship of pulmonary surfactant protein D( SP-D) with chronic obstructive pulmonary disease ( COPD) by measuring SP-D level in serum and lung tissue of rats with COPD.Methods The rat COPD model was established by passive smoking as well as intratracheal instillation of lipopolysaccharide ( LPS) . Thirty male SD rats were randomly divided into a control group, a LPS group, and a COPD group( n =10 in each group) . The pathologic changes of lung tissue and airway were observed under light microscope by HE staining. Emphysema changes were evaluated by mean linear intercept ( MLI) of lung and mean alveolar number ( MAN) . The level of SP-D in serum was measured by enzymelinked immunosorbent assay ( ELISA) . The expression of SP-D in lung tissue was detected by Western-blot and immunohistochemistry.Results The MLI obviously increased, and MAN obviously decreased in the COPD group compared with the control group ( Plt;0.05) . There was no significant difference in the MLI and MAN between the LPS group and the control group ( Pgt;0.05) . The serum SP-D level was ( 49.59 ±2.81) ng/mL and ( 53.21±4.17) ng/mL in the LPS group and the COPD group, which was significantly higher than that in the control group [ ( 42.14±2.52) ng/mL] ( Plt;0.05) . The expression of SP-D in lung tissue was 0.56±0.01 and 0.63±0.01 in the LPS group and the COPD group, which was also obviously ber than that in the control group ( 0.39 ±0.01) ( Plt;0.05) .Meanwhile the SP-D levels in serumand lung tissue were higher in the COPD group than those in the LPS group ( Plt;0.05) . The levels of SP-D between serum and lung tissue were positively correlated in all three groups ( r=0.93, 0.94 and 0.93, respectively, Plt;0.01) .Conclusion Both the SP-D level in serum and in lung tissue increase significantly in COPD rats and correlate well each other, which suggests that SP-D may serve as a biomarker of COPD.
Objective To investigate the protective effects of endotoxin pretreatment on lung injury of rats with endotoxemia. Methods The rat model of acute endotoxemia was established by injecting lipopolysaccharide (LPS) intraperitoneally. Seventy-two male Wistar rats were randomly divided into three groups, ie. a saline control group (N, n=24) , a LPS-treated group (L, n=24) , and a LPS pretreated group ( P, n=24) . Each group was divided into 2 h, 4 h, 6 h, and 12 h subgroups. The rats in group P were firstly administered with introperitoneal injection of 0.25 mg/kg LPS. After 24 hours, they were subjected to the injection of 0.5 mg/kg LPS. The rats in group N and L received injection of equivalent amount of saline. After 72 hours, the rats in group L and P were challenged with intravenous injection of 10 mg/kg LPS, otherwise saline in group N. Six rats were killed at 2, 4, 6 and 12 hours respectively after injection of LPS in group L and P. The lungs were removed for detecting intercellular adhesion molecule-1 ( ICAM-1) , superoxide dismutase ( SOD) , and malondialdehyde (MDA) . Meanwhile the level of tumor necrosis factoralpha ( TNF-α) in serum was measured, and the pathological changes of lung were also examined. Results The contents of ICAM-1, MDA and TNF-α in the LPS-treated 4 h group were 75.07 ±0. 53, ( 3.93 ± 0.42) μmol/g, and (478.62 ±45.58) pg/mL respectively, significantly higher than those in the saline control group. The endotoxin pretreatment reduced the above indexes to 42.40 ±0.44, ( 2.89 ±0.49) μmol / g and ( 376.76 ±43.67) pg/mL respectively (Plt;0.05) . The content of SOD in the LPS-treated 4 h group was ( 6.26 ±0.31) U/mg, significantly lower than that in the saline control group. The endotoxin pretreatment increased SOD to ( 8.79 ±0.35) U/mg. Conclusion Endotoxin pretreatment can suppress the progress of lung injury in rats with endotoxemia and protect the lung tissue by down-regulating the inflammatory response and oxygen free radical production.
ObjectiveTo study the changes of lipopolysaccharide binding protein (LBP) in the serum of Wistar rats with obstructive jaundice and to investigate its potential mechanism.MethodsEighty male Wistar rats were randomly divided into obstructive jaundice group (OJ group, n=40） and sham operation group (SO group, n=40）. Before operation and the 5th, 10th, 15th, 20th day after common bile duct ligation, the levels of LBP, endotoxin, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in plasma were detected in all the rats. ResultsLBP levels in serum increased significantly in OJ group on the 10th day after operation compared with those of SO group. Moreover, LBP levels gradually increased in OJ group with the prolongation of obstructive time. A positive correlation existed between serum LBP and plasma endotoxin, TNF-α and IL-6.ConclusionThe study demonstrates that LBP in serum is high and plays an important role in the pathogenesis of multiple organ injury secondary to obstructive jaundice. It may be an appropriate way to treat patients with obstructive jaundice by decreasing LBP levels in serum.
We established acute cholangitis and endotoxiemia in 18 rabbits by ligating the common bile duct and injecting E coli(O111B4 strain)into the common bile duct. After perfusion through activated charcoal via femoral artery-vein pathway, the average blood levels of endotoxin decreased sighificantly from 2.24Eu/ml to 0.17Eu/ml(Plt;0.001). This result suggested that blood perfusion through activated charcoal may be a promising therapy for acute endotoxemia.
【Abstract】Objective To investigate the preventive role of selective decontamination of the digestive tract (SDD) in gut-originated endotoxemia in acute necrotizing pancreatitis (ANP). Methods A lethal model of ANP was reproduced in Wistar rats by retrograde infusion of artificial bile into the main pancreatic duct. Normal control group (n=6), sham operation group (n=6), ANP group (n=14) and ANP+SDD (polymycin E, tobramycin and nystatin mixture) group (n=8) were randomly devided. Visceral pathologic changes, serum levels of TNFα and IL-1β, intestinal bacterial flora, plasma D(-)lactate and endotoxin contents, as well as the mortality were examined at 72h after operation in each group. Results Necrosis and inflammation of pancreas, with a remarkable elevation of serum TNFα and IL-1β and intestinal flora disturbance (with E.Coli content risen significantly) were seen in ANP rats. Simultaneously, ANP rats displayed elevated plasma concentration of D(-)lactate and endotoxin. In SDD group, enterobacteraceae and yeast were markedly depressed, while anaerobes were well preserved, with the value of B/E 〔Bifidobacterium/E.Coli, log10(CFU/CFU）〕 elevated in the ileac mucous membrane (1.73±1.23 vs -0.37±0.72 in ANP group,P＜0.01) and in the caecum content (∞ vs 0.88±0.77). In addition, depressed levels of D(-)lactate 〔（3.95±1.83） mg/L vs （8.05±3.05） mg/L in ANP group,P＜0.01〕, endotoxin 〔（0.227±0.084） EU/ml vs （0.423±0.155） EU/ml in ANP group, P＜0.01〕 and TNFα 〔（15.41±10.32） ng/L vs （46.79±24.31） ng/L in ANP group P＜0.01〕 in systemic or portal vein were observed in the SDD group. Moreover, SDD group displayed a declined 72h mortality(14.3% vs 58.8% in ANP group, P=0.005). Conclusion ANP is associated with gut barrier disorder and gut flora imbalance, which may exacerbate the process of gut-originated endotoxin translocation. By protecting gut flora and gut barrier against disorder, SDD attenuates ANPrelated endotoxemia and improves the outcome. SDD is advisable for the prophylaxis of gut-originated endotoxemia complicated from ANP.
PURPOSE:To investigate and changes of the retina and the chorid induced by lipopolysaccharide (LPS)in Lewis rats and to compare the results obtained on tissue wholemounts and sections. METHODS:Immunohistochemistry was carried out both on wholemounts of the retina and the chorid-sclera complex and on ocular sections from normal Lewis rats and those after LPS injection. RESULTS:It was shown on the tissue wholemounts that monocytes were attached to retinal blood vessels and emigrated into the choroid as early as 4hrs after LPS injection. Severe involvement of the retina and macrophages into whole area of these tissues.Furthermore increasing number of major histocompatibility complex classⅡ(MHC classⅡ)positive cells was observed in the choroid.The results on tissue sections revealed that the retina and the choroid were both involved as videnced by infiltration of these cells at some time points after LPS injection. CONCLUSION:Wholemount technique provides undoubtful evidences to show that the retina and choroid are primarily and severely involuted after LPS injection.The endotoxin induced uveitis is,for the first time,presumed to be model for human generalized uveitis. （Chin J Ocul Fundus Dis,1996,12:33-36）
TO investigate the relationship between endotoxemia and structural change in the pancreatic tissue and therapeutic effects of naltrexone (NTX) on experimental acute hemorrhagic necrotizing pancreatitis in rats. The model of acute hemorrhagic necrotizing pancreatitis (AHNP) of rats was induced by retrograde injection of 5% sodium taurocholate into the pancreatic duct. One hundred and ten Wistar rats were randomly divided into three groups: control group (n=20),AHNP group (n=45) and NTX treatment (n=45) group. The weight of pancreas and plasma levels of amylase and endotoxin were measured as well as changes of the pancreatic histology were examined by light and electric microscope in 6h, 12h, 24h after operation. Results as compared with control groups , amylase and endotoxin in AHNP group were significantly higher in the plasma and the damage to pancreatic tissue was increased in severity as observed with light and electric microscopes in 6h, 12h, 24h after operation. Comparison between NTX treatment groups with AHNP groups demonstrated that amylase and endotoxin were significantly decreased in the plasma, and the damage to pancreatic tissue was reduced in NTX treatment phase. Conclusion these results showed that endotoxemia was induced by AHNP, but NTX decreased the edotoxin level in the plasma and improved the damage of pancreatic tissue. The lethality was significantly lowered and average survival time was prolonged during NTX treatment of AHNP.
Objective To investigate the expression of granulysin ( GNLY) in lung of rats with acute lung injury ( ALI) stimulated with lipopolysaccharide ( LPS) . Methods Thirty-six healthy adult Wistar rats were randomly divided into a normal control group and a LPS group, with 18 rats in each group. LPS ( 4 mg/kg) was given intraperitoneally in the LPS group to induce ALI. The same amount of normal saline was given in the control group. The rats were randomly assigned to three subgroups ( n = 6) to be sacrificed respectively at 6, 18, and 30 hours after intraperitoneal injection. Wet/dry lung weight ratio ( W/D) and pathological changes of the lung were observed. The expression of GNLY in lung tissue was assayed by immunohistochemistry. Results In the LPS group, the W/D ratio was higher than that of the control group at each time point ( P lt;0. 05) and there were a large number of inflammatory cells infiltration and edema in interstitial spaces which suggested ALI. Compared with the control group, the expression of GNLY in the LPS group was significantly increased at all time points ( P lt;0. 05) . Conclusion GNLY may participate in ALI inflammatory process, which might play a role in preventing infection induced ALI.
Kupffer cell phagocytic function and plasma endotoxin level in 36 patients with obstructive jaundice were observed. The results indicated that kupffer cell phagocytic function was inhibited and the plasma endotoxemia level was markedly increased as compared with those in the control group Ｐ＜0.05 and Ｐ＜0.01 respectively. Kupffer cell phagocytic function were recoverd and plasma endotoxemia alleviated while the biliary obstruction was released by surgery.