Objective This study was to evaluate the effects of growth hormone (GH) on cell apoptosis of intestinal epithelium in acute necrotizing pancreatitis (ANP) rats.Methods Seventy-two SD rats were divided into three groups randomly: sham operation (SO) group, ANP group, and GH treatment group. GH-treatment group received subcutaneously 0 75?U/kg of GH. At 3?h, 6?h, 12?h, and 24 ?h after induction of ANP, the small intestinal specimens were harvested and apoptosis of intestinal epithelium was studied by DNA gel electrophoresis, FCM and TUNEL method. FasL and Bax protein expressions were detected by immunohistochemistry.ResultsThe ladder pattern on DNA gel electrophoresis presented in all time points of ANP group, but only seen in GH-treated group at 3h. Apoptotic percentage significantly increased in ANP group [(50?11)%,(80?9)%,(48?17)%,(50?10)%] as compared with SO group [(54?4)%, (28?6)%, (39?5)%,(29?11)%], all P

Objective To investigate the deleterious effects of enterogenous endotoxemia on the course of acute pancreatitis in mice, and its possible mechanisms. Methods Sixty five C57BL/6 mice were assigned to 4 groups randomly, including acute edematous pancreatitis (AEP), lipopolysacchride (LPS), AEP plus LPS and normal control. AEP was induced by intraperitoneal injection of cerulein with a dosage of 50 ?g/kg at hourly interval for seven times under ether anesthesia. LPS was administrated via a gastric tube with a dosage of 5 mg/kg at 6 h after the first cerulein or saline injection. Serum amylase and LDH activities were measured at 12 h, 24 h, 48 h and 5 d. Pathological alteration in pancreas was studied. Expressions of Mac 1 (CD11b/CD18), P selectin, E selectin and ICAM 1 were evaluated by using inmmunohistochemical procedures. Expressions of cytokine genes were determined by means of RT PCR and Southern blot. Myeloperoxidase (MPO) activity in pancreas was also analyzed. Results Cerulein induced a typical changes of AEP in mice, which was confirmed by pathological changes and hyperamylasemia. LPS alone didn't develop either morphological changes or biochemical alterations. However, cerulein induced AEP challenged by LPS could cause marked parenchymal necrosis and hemorrhage with significant increment of serum amylase and LDH activities. Expressions of Mac 1, P selectin, E selectin and ICAM 1 in pancreas were enhanced. Cytokine genes including TNF?,IL 1?,IL 6 and IFN? mRNA were also upregulated. MPO activity was increased. Conclusion This study suggested that enterogenous endotoxemia, which could not induce pancreatic injury per se , could induce AEP into ANP in mice. Over stimulation of neutrophils and releasing of pro inflammatory mediators might be the contributing factors.

Objective To investigate whether apoptosis of intestinal epithelial cells occurs at the early stage of acute necrotizing pancreatitis (ANP) in rats. Methods Fourty eight Spraque Dawley rats were used. ANP model of rats was induced by retro injection of 5% sodium taurocholate into biliopancreatic duct. Laparotomized animals without induction of ANP (sham operation) served as controls. The distal segment of ileum specimens were harvested at 3 h, 6 h, 12 h and 24 h after operation and the apoptosis of intestinal epithelial cells was studied by DNA gel electrophoresis, FITC conjugated annexin V and propidium iodide (PI) staining cells analyzed by Flow Cytometry (FCM) and immunohistochemical procedures (TUNEL method). Results The DNA electrophoresis showed that typical “ladder” patterns appeared at all indicated time points in ANP group, while the DNA specimens from control group presented a single chromosomal lane, except the one at 12 h. Apoptotic percentage of detached intestinal epithelial cells assayed using Annexin V kit by FCM were (53.7?3.7)%, (27.6?6.0)%, (39.0?4.8)%, (29.0?11.3)% at 3 h, 6 h, 12 h and 24 h in control group and (50.3?11.3)%, (79.7?9.2)%, (47.8?17.3)%, (49.6?9.5)% in ANP group. There was a significant difference between two groups at 6 h, P

Objective Some experimental results indicated that cyclooxygenase 2 (COX 2) was involved in the regulatory process of balance between cell apoptosis and multiplication. The present study was designed to investigate the effect of COX 2 on the course of pancreatic adenocarcinoma cell apoptosis and its possible signal pathway. Methods Apoptosis of pancreatic cancer cells (PC 3, highly expressed COX 2) induced by selective COX 2 inhibitor, Celebrex (IC 50 , 100 ?mol), was detected by using DNA gel electrophoresis, flow cytometry and electron microscopy. Expressions of apoptotic related genes mRNA, including bcl xl, bax, Survivin, were analyzed by reverse transcription polymerase chain reaction (RT PCR). Results Substantial apoptosis was induced by the treating PC 3 cells with Celebrex, as revealed by typical ladder pattern of DNA fragments under DNA electrophoresis, increment of apoptotic apportion, and apoptotic body under electron microscopy. Apoptotic inhibitory genes, bcl xl, bax, Survivin, were expressed in PC 3 cells, and were down regulated significantly by Celebrex in bcl xl and Survivin but not for bax. Conclusion Above findings suggest that the COX 2 pathway contributes to the apoptosis of pancreatic cancer cell, which may be via signal transduction of bcl xl and Survivin genes.

Objective To investigate the effect of pancreatic stellate cells on invasion and metastasis of human pancreatic cancer cell AsPC-1,and to determine the role of SDF-1 in this process.Methods PSCs were routinely isolated and cultured,and PSCs conditioned media(PSC-CM) was collected and concentrated.Different concentrations of PSC-CM,anti SDF-1 and their combination were used to treat AsPC-1 cells,and MTT assay was applied to detect the proliferation of pancreatic cancer cells.Transwell chamber migration assay was employed to detect the migration of AsPC-1 cells.In vitro invasion assay was used to determine the invasion of AsPC-1 cells.Results A490 values of AsPC-1 cell in control group and 0.25,0.5,1 μg/lμl PSCCM group were 0.437 ±0.041,0.472 ±0.048,0.553 ±0.057,0.690 ±0.051,and PSC-CM promoted cell proliferation in a dose dependant manner.The difference between 0.5,1 μg/μl PSC-CM group and control group,and between 1 μg/l and 0.5 μg/μl PSC-CM group was statistically significant (P＜0.05).A490 values of control group,anti SDF-1 group,PSC-CM group and PSC-CM ± anti SDF-1 group were 0.407 ±0.028,0.416 ±0.030,0.629 ±0.048,0.481 ±0.049.The numbers of penetrating cells were 35.3 ±7.1,34.8±5.6,140.9 ± 12.7,56.5±5.9,and the numbers of invasive cells were 27.1 ±2.9,29.1 ±4.2,81.5 ±8.2,46.4 ± 4.4.The difference between anti SDF-1 group and control group was not statistically significant.The proliferation,migration and invasion of pancreatic cancer cells in PSC-CM group was significantly higher than those of control group (P ＜0.05 or P ＜0.01).The proliferation,migration and invasion of pancreatic cancer cells in PSC-CM ± anti SDF-1 group was significantly lower than those of PSC-CM group,but they were significantly higher than those of control group (P ＜ 0.01).Conclusions PSCs can promote proliferation,migration and invasion of pancreatic cancer cells AsPC-1,and the mechanism may be partly due to SDF-1/CXCR4 receptor ligand axis.

Hospital TQM system is designed to fit China′s specifics,based on the Total Quality Management (TQM)theory and integrating the system theory concepts, comprising two structural modules of perceived quality and non-perceived quality.The former is a trinity framework made up of patient satisfaction,employee commitment and social reputation,while the latter is a management system featuring“Six pillars and six columns”,constituting a three-dimensional management for integrated operation and integration of the hospital.

The effects of tetramethylpy-razine (TMP) on pancreatic blood flow and survival rate were studied in sodium tarocholate-in-duced acute pancreatitis (AP) in rats. The results showed that pancreatic relative blood flow and pancreatic tissue perfusion were significantly increased and the pathologic changes and survival rate were improved in TMP treated group-s. Plasma value of TXB2?6-Keto-PGF1? and platelet aggregation rate (PAR) were also mea-sured. We found that TMP could maintain the balance between TXA2 and PGI2 and lower the elevated PAR. It was suggested that TMP has therapeutic effect on AP in rats through improving pancreatic microcirculation; which was related to the maintanance of the balance between PGI2 and TXA2.

AIM To investigate the effects and possible mechanism s of Glycyrrhizin on rat pancreatic fibrosis induced by TNBS (trinitrobenzenesulfonic acid, TNBS ). METHODS Chronic pancreatitis model was induced in male Sprague -Dawley rats by injection of 2% TNBS into bile duct. All the rats were randomly divided into two groups. The rats in Glycyrrhizin intervention group were treat ed with Glycyrrhizin 8 mg?kg -1 by injection into tail vein from day 3 to day 28, while the rats in control group were administrated with same volume of saline vehicle. Ten rats in the Glycyrrhizin intervention group and eight rats in the control group wer e sacrificed on day 29, the blood was collected to determine amylase and hyaluro nic acid by enzyme dynamic and RIA method. The histological change of pancreatic tissue was evaluated by H&E stain and modified Van-Gieson stain. Mast cell in pancreas was stained by thionine blue. Expression of TGF-? 1,Collagen Ⅰ and ?-SMA in pancreas were assessed by immunohistochemistry and western blot. RESULTS In the Glycyrrhizin intervention group, the mast cell number and the percentage of degranulation decreased significantly, and the expression of ?-SMA protein also decreased compared to the control group, but there was no difference in amylase or hyaluronic acid between the treatment group and the control group. In the Glycyrrhizin intervention group, inflammation and fibrosis were ameliorated and expression of collageⅠ and TGF-? 1 was also decreased significantly compared to the control group. CONCLUSION Glycyrrhizin inhibits pancreatic fibrosis in chronic pancreatitis rats induced by TNBS. This action might be related to protecting pancreatic acinus cells from being destructed by mast cell activation and inhibiting extracellular matrix synthesis stimulated by pancreatic stellate cell.

Objective To investigate the effects of cyclooxygenase-2 (COX-2) on the expressions of vascular endothelial growth factor (VEGF) and prostaglandin E_2 (PGE_2) in pancreatic carcinoma both in vitro and in vivo, and to clarify the possible mechanism of PGE_2 in mediating COX-2 inducing angiogenesis of pancreatic carcinoma. Methods In vitro study, the inhibitory effects of Celebrex, a selective cyclooxygenase-2 inhibitor, on the expression of VEGF and PGE_2 in pancreatic carcinoma cell lines PC-3 were determined using either enzyme-linked immuno-absorbent assay (ELISA) or radioimmunoassay (RIA). Effect of exogenous PGE_2 on the down-regulation of VEGF by Celebrex was also assessed. In vivo study, PC-3 cell line xenograft nude mice model was established. Changes of VEGF expression and PGE_2 of tumor tissues after the treatment of Celebrex were investigated using Western blotting or RIA. Results Celebrex suppressed the expressions of VEGF and PGE_2 in cultured PC-3 cell line with a manner of dose- and time-dependence. Exogenous PGE_2 up-regulated the expression of VEGF, which was suppressed by Celebrex in a dose-dependent fashion. In vivo study, administration of Celebrex into xenograft nude mice inhibited expressions of VEGF and PGE_2 significantly. Conclusion COX-2 is involved in angiogenesis in pancreatic carcinoma probably through the inhibition of the production of angiogenic factors such as VEGF. PGE_2 is likely to act as an important mediator in this process.

Objective To evaluate the protective effect by inhibiting nuclear factor-kappa B (NF-?B) by N-acetyl-L-cysteine(NAC) on donor rat lung. Methods 24 SD rats were randomly divided into two groups, the control group and the experiment group. The harvested lung blocks were flushed with and stored in the low-potassium-dextran (LPD) solution in control group, but in the experiment group, LPD solution containing NAC was used. The lungs were preserved at 4℃ for 16 hours in both groups. Isolated rat lung reperfusion models were established and the donor lungs were perfused for 1 hour. PaO_2 and 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) and nuclear factor-kappa B(NF-?B) were also observed by using immunohistochemistry and semi-quantitative RT-PCR at the end of reperfusion. Results After reperfusion for 60 minutes, in experiment group, PaO_2 drop in and increase PAwP lower than in control group (P