【Abstract】 Objective To investigate the protective role of recombinant human growth hormone (rhGH )in ischemic reperfusion injury of rat liver and its mechanism. Methods One hundred Male rats were randomly divided into two groups: the rhGH group and the control group. In the rhGH group, rhGH were injected （0.2U/100g weight） to rats seven days before the ischemic reperfusion injury, and in the control group, normal saline was injected instead. Serum levels of ALT， TNF-α and IL-1α were tested. Hepatic tissue was sectioned for to detect the level of EC and MDA, the expression of NF-κB and ICAM-1 mRNA on SEC. Ultrastructural characteristics histopathological characteristics were determined also. Results Serum levels of ALT, TNF-α, IL-1α and the contents of MDA in the control group were significantly higher than those in the rhGH group （P＜0.05）. Comparied with control group, rhGH also decreased NF-κB activation, and reduced the expression of ICAM-1 mRNA of SEC in the liver cells （P＜0.05）. Electronic microscopic revealed that the hepatic sinusoidal endothelial cells and the hepatocellular mitochondria were injured in the control group. Pretreatment with the rhGH was able to significantly improved the pathological changes. Conclusion rhGH might confer the protection to ischemic reperfusion injury of rat liver through reducing the expression of NF-κB to down-regulate cytokine (IL-1α,TNF-α), MDA and inhibition the expression of ICAM-1 mRNA.
【Abstract】Objective To investigate the effects of human interlukin-13 (hIL-13) on the expression of E-selectin and intercellular adhesion molecule-1(ICAM-1) on bovine aortic endothelial cells(BAECs) stimulated by tumor necrosis factor alpha(TNF-α), and to provide experimental basis for hIL-13 inducing immunity endure and relieving the repulsion reaction of xenograft. Methods BAECs were co-cultured with different concentrations of hIL-13 for 2 h and followed by co-cultured with 4 ng/ml TNF-α for 6 h or 18 h. The expressions of E-selectin and ICAM-1 on BAECs were detected by Cell-ELISA. The effect of hIL-13 on activity of BAECs was detected by MTT colorimetry.Results BAECs pretreateded with hIL-13 could inhibit the expression of E-selectin and ICAM-1 induced by TNF-α, and showed a doesdependent manner from 5 ng/ml to 20 ng/ml of hIL-13 (P＜0.01). The experimental result of BAECs activity measured by MTT proved no significant difference in the activities of BAECs in every experimental groups compared with control group’s. Conclusion hIL-13 could inhibit the expression of E-selectin and ICAM-1 on BAECs induced by TNF-α, which may contribute to the xenotransplant immune tolerance.
Objective To observe the protective effect on rat lung by using N-acetyl-L-cysteine(NAC) a inhibiter of nuclear factor-kappa B (NF-κB) in the period of reperfusion. Methods Twenty-four rats were randomly divided into a control group and a trail group.The harvested lung blocks of 12 rats were flushed with and stored in the low-potassium-dextran (LPD) solution at 4℃ for 16 hours. The isolated rat lung reperfusion models were established and the donor lungs were perfused for 1 hour. NAC was used in the trail group but normal saline was used in control group. Partical pressure of oxygen in artery (PaO2), peak airway pressure (PawP) were measured at every 15 min intervals during reperfusion. After reperfusion, the lung tissue wet-to-dry(W/D)ratio, and myeloperoxidase(MPO) activity were obtained. The protein and mRNA expressions of intercellular adhesion molecule-1(ICAM-1), NF-κB were also observed by using immunohistochemistry and semi-quantitative RT-PCR at the end of reperfusion. Results The level of decreased PaO2 and increased PawP in trail group were lower than those in control group at every interval time the sample obtained after reperfusion in 60 min. (Plt;0.01 or lt;0.05). After reperfusion the W/D,MPO, the protein and mRNA expressions of ICAM-1, NF-κB were decreased evidently in trail group than those in control group(Plt;0.01 or lt;0.05). Conclusion Using NAC in the period of reperfusion, can effectively inhibit the expression of NF-κB and ICAM-1,further improve lung respiratory functions.
ObjectiveTo study the clinical value of changes of serumα-fetoprotein(AFP) and soluble cell adhesion molecule-1(sICAM-1) levels before and after surgical treatment of primary hepatocellular carcinoma(PHC) as predictors of patient survival. MethodsThe clinical data and followed-up results of 86 patients with hepatocellular carcinoma received hepatectomy or radiofrequency ablation(RFA) in Xijing Hospital and the 451st Hospital of PLA were retrospectivly analyzed. The changes of peripheral blood AFP and sICAM-1 levels in patients before and in 1 month after treatment were observed and all patients were divided into different groups according to the changes in both two markers. Then survival rates of each group were analyzed. ResultsThe patients with AFP < 20μg/L or sICAM-1 < 1 000 U/L before treatment had lower tumor recurrence rate and higher survival rate than patients with elevated serum levels of the both markers(AFP:P=0.018, P < 0.001;sICAM-1:P=0.027, P < 0.001). The larger tumor, late TNM stage, and higher rate of recurrence were associated with elevated serum levels of the both markers(AFP:P=0.016, P=0.026 and P=0.025;sICAM-1:P < 0.001, P=0.024 and P=0.032). The better survival situation was closely related with these cases treated with hepatectomy and their levels of both markers were lower than the above cutoff values both before and after treatment, or leves of both markers above the cut-off values returned to within the normal range after treatment (AFP:P=0.006, P=0.001;sICAM-1:P=0.001, P=0.002). The patients who had simultaneous increase of AFP and sICAM-1 after operation showed the worst tumor-free and overall survivals(P=0.007, P < 0.001). ConclusionTo test the changes of serum AFP and sICAM-1 levels in early stage after treatment for patients who received radical resection of hepatocellular carcinoma has good clinical value for monitoring of tumor recurrence and predict prognosis.
ObjectiveTo investigate the protective effect of Roux-en-Y gastric bypass surgery on early damage of renal tissue in type 2 diabetes mellitus rats, and explore the mechanism of the protective effects. MethodsDiabetes mellitus animal models were induced by intraperitoneal injection of streptozotocin (STZ, 35 mg /kg) and a high-fat diet.Diabetic rats were divided into three groups randomly (digital table method): diabetes control group (n=8), sham operation group (n=8), and Roux-en-Y gastric bypass group (n=14).Another 8 normal SD rats as the normal control group.The fasting blood glucose, serum total cholesterol (TC), triglyceride (TG), and free fatty acid (FFA) were measured before operation and in 8 weeks after operation; plasma BUN and Cr were measured respectively before operation and in 4 and 8 weeks after operation in each group rats, 24 h urine microalbumin and urine 8-hydroxydeoxyguanosine were measured respectively before operation and in 8 weeks after operation in each group rats.Renal pathological changes were observed and the indexes of kidney hypertrophy, the mean glomerular area (MGA), and the mean glomerular volume (MGV) were analyzed in 8 weeks after operation.The expressions of fibronectin, typeⅣcollagen (CoⅣ), transforming growth factor-β1 (TGF-β1), intercellular adhesion molecule-1(ICAM-1), nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), and Bcl-2 protein in renal tissues were investigated by immunohistochemical staining. ResultsRoux-en-Y gastric bypass surgery could reduce the blood glucose, blood lipid, MGA, MGV, and the index of kidney hypertrophy of diabetic rats significantly (P < 0.05), improved renal pathological morphology and kidney function (P < 0.05), reduced the protein expressions of fibronectin and CoⅣ, decreased the protein expressions of TGF-β1, ICAM-1, and NOX4, and increased the protein expression of Bcl-2. ConclusionRoux-en-Y gastric bypass surgery can improve kidney function and the pathological damage of diabetes rats, its mechanism may be related to inhibition the protein expressions of TGF-β1, ICAM-1, and NOX4, and increase the protein expression of Bcl-2.
Objective To investigate the targeted combination and anti-inflammatory effects of anti-intercellular adhesion molecule 1 (ICAM-1) targeted perfluorooctylbromide (PFOB) particles on myocardial ischemia-reperfusion injury in rat model. Methods Seventy-six adult Sprague Dawley rats (male or female, weighing 250-300 g) were selected for experiment. The models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery for 30 minutes in 30 rats. The expression of ICAM-1 protein was detected by immunohistochemistry staining at 6 hours after reperfusion, and the normal myocardium of 10 rats were harvested as control; then the content of interleukin 8 (IL-8) in serum was tested every 6 hours from 6 hours to 48 hours after reperfusion. The other 36 rats were randomly divided into 6 groups (n=6): ischemia-reperfusion injury model/targeted PFOB particles group (group A), ischemia-reperfusion injury model/untargeted PFOB group (group B), normal control/targeted PFOB particles group (group C), normal control/untargeted PFOB particles group (group D), ischemia-reperfusion injury model/normal saline group (group E), and sham operation group (group F). The ischemia-reperfusion injury models were established in groups A, B, and E; while a thread crossed under the coronary artery, which was not ligated after open-chest in group F. After 6 hours of reperfusion, 1 mL of corresponding PFOB particles was injected through juglar vein in groups A, B, C, and D, while 1 mL of nomal saline was injected in group E. Ultrasonography was performed in groups A, B, C, and D before and after injection. The targeted combination was tested by fluorescence microscope. The content of IL-8 was tested after 6 and 24 hours of reperfusion by liquid chip technology in groups A, B, E, and F. Results After 6 hours of reperfusion, the expression of ICAM-1 protein significantly increased in the anterior septum and left ventricular anterior wall of the rat model. The content of IL-8 rised markedly from 6 hours after reperfusion, and reached the peak at 24 hours. Ultrasonography observation showed no specific acoustic enhancement after injection of PFOB particles in groups A, B, C, and D. Targeted combination was observed in the anterior septum and left ventricular anterior wall in group A, but no targeted combination in groups B, C, and D. There was no significant difference in the content of IL-8 among groups A, B, and E after 6 hours of reperfusion (P gt; 0.05), but the content in groups A, B, and E was significantly higher than that in group F (P lt; 0.05). After 24 hours of reperfusion, no sigificant difference was found in the content of IL-8 between groups A and B (P gt; 0.05), but the content of IL-8 in groups A and B were significantly lower than that in group E (P lt; 0.05). Conclusion Anti-ICAM-1 targeted PFOB particles can target to bind and pretect injured myocardium of rat by its anti-inflammation effects.
ObjectiveTo investigate the effects and clinical significance of edaravone on serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) in elderly patients with obstructive sleep apnea hypopnea syndrome (OSAHS).MethodsA total of 90 elderly patients with moderate to severe OSAHS confirmed by polysomnography were recruited from North China University of Science and Technology Affiliated Hospital in February 2016 to October 2017. According to random number table method the OSAHS patients were randomly divided into group A (n=30), group B (n=30) and group C (n=30). Group A received continuous positive airway pressure treatment for six months, group B received edaravone therapy and continuous positive airway pressure treatment for six months, and group C only received edaravone therapy for six months. The changes of serum TNF-α, IL-6 and ICAM-1 were detected by enzyme-linked immunosorbent assay before and after treatment.ResultsThe differences of serum TNF-α, IL-6 and ICAM-1 before treatment in the three groups were not statistically significant (P>0.05). Compared with before treatment, the levels of serum TNF-α, IL-6 and ICAM-1 decreased in the three groups (P<0.05). After six months of treatment, the levels of serum TNF-α, IL-6 and ICAM-1 decreased in group A and group B compared with group C (P<0.05), and decreased significantly in group B compared with group A (P<0.05).ConclusionEdaravone can inhibit the expressions of serum TNF-α, IL-6 and ICAM-1 in elderly patients with moderate to severe OSAHS, and thereby reduce vascular endothelial dysfunction and injury.
Objective To explore the effect and mechanism of glutamine to the aberrant crypt foci (ACF) in rat injured by acetic acid. Methods Thirty Wistar rats were averagely divided into three groups: control group, acetic acid group and glutamine group. The colon of the rat was infused with 1% acetic acid. Started to gavage with glutamate two days after modeling glutamine group. The injured colons were studied after fourteen days with light and scanning electronic microscope. Paraffin sections of specimens were prepared and stained with HE. The colon crypts were isolated by HCl digestion method. The expressions of CD44 and ICAM-1 in the epithelial cell of the large intestine mucosa were detected by immunohistochemistry method. Results On the days of 14， the number of ACF in the glutamine group were remarkably decreased as compared with that of the acetic acid group and a branch-like. The expressions of ICAM-1 and CD44 (every 1 000 cells) were 302.1±30.1 and 298.6±28.3 in glutamine group, 223.6±23.5 and 221.5±28.6 in control group, 198.5±19.5 and 215.3±17.8 in acetic acid group, respectively. While the expressions of CD44 and ICAM-1 in intestine were increased remarkably in the glutamine group compared with the control group and acetic acid group (P＜0.05). Conclusion Glutamine could decrease the formation of the ACF injured by acetic acid. Increasing the expressions of CD44 and ICAM-1 may be one of the important factors to decrease the ACF.
目的 探讨异氟醚通过抑制细胞间黏附分子（ICAM-1）表达参与减轻肝脏缺血-再灌注（IR）损伤的可能调节机制。 方法 32只雌性SD大鼠分为4组。A组大鼠行腹腔注射1%戊巴比妥钠40 mg/kg麻醉，进行手术但不阻断入肝血流；B组1%戊巴比妥钠麻醉后行部分肝脏IR；C组大鼠仅接受1.0 MAC异氟醚吸入麻醉，不阻断血流；D组采用1.0 MAC异氟醚麻醉，建立肝脏IR模型。肝脏缺血60 min，再灌注3 h后取肝组织和血液标本，检测血清丙氨酸转氨酶（ALT）和天冬门氨酸转氨酶（AST）、肝组织ICAM-1和肝组织还原型谷胱甘肽（GSH）、脂质过氧化物丙二醛（MDA）和超氧化物歧化酶（SOD）含量。 结果 与戊巴比妥钠麻醉比较，采用异氟醚处理后明显降低血清ALT和AST的水平，再灌注肝组织内GSH、SOD含量明显高于而MDA含量降低，同时抑制肝组织ICAM-1的表达。 结论 异氟醚麻醉能够有效减轻肝脏IR损伤，抑制氧自由基的生成和释放，具体机制可能与抑制ICAM-1表达致使细胞内GSH含量增加密切相关。