Gut microflora , an important part in maintaining the intestinal homeostasis , can participate in the development of intestinal mucosal immune system , promote the synthesis of secreted IgA ( sIgA) and interact with intestinal immune cells .Gut micro-flora also plays a significant role in the development of inflammatory bowel diseases , irritable bowel syndrome , pediatric allergic disea-ses and other disorders .This paper reviews the advances about the correlation of gut microflora and intestinal mucosal immunity .

To explore the significance of endothelin-1 converting enzyme (ECE-1)mRNA expression in the development and progression of stress ulcer in cold-restraint-stress(CRS) rats, a model was established by CRS-induced ulcers in rats. ET-1 contents in plasma and gastric mucosa of rats were measured by using radioimmunoassay(RIA)method, gastric mucosa blood flow(GMBF) in rats were determined by using laser-doppler flowmetry, ulcer index(UI) in rats was estimated according to"Guth standard", and the expression levels of ECE-1mRNA in gastric mucosa of normal and CRS rats were measured by using dot blot and reverse transcription-polymerase chain reaction(RT-PCR). The results indicated that compared with control values,the ET-1 contents in both plasma and gastric mucosa of CRS rats were increased significantly after stress (P

Objective To compare the gastric mucosa damage induced by celecoxib and conventional NSAIDs——indomethacin. Methods NSAIDs induced gastric mucosal damage model in rats was obtained by pouring indomethacin, celecoxib respectively (n=8); After gastric damage induced by means of 100% ethanol, celecoxib were administered by gastric gavage (n=8). Gastric mucosal 6-keto-PGF 1? ,TXB 2 level and lesion index (LI) were measured. Morphological changes of gastric mucosa were assessed under light and scanning electronic microscopy. Results Indomethacin caused obvious gastric damage (LI:13.38?2.06) and a marked reduction of 6-keto-PGF 1? ,TXB 2 level was observed (P

The aim of the study was to demonstrate the influence of immersion and restraint stress on the ultrastructural changes in gastric acid barrier and parietal cells in rats. Twenty rats were randomly divided into control and stress groups. The gastric mucosal ulcer index was measured. The ultrastructural changes in parietal cells, epithelial cells, epithelial cell junctions, and basal lamina were observed by transmission electronic microscopy. Stress could induce gastric mucosal damage obviously. Parietal cells in a resting state in control group but became active in stress groups with plenty of mitochromosomes and secreting cysts. The cell membrane of epithelium on the luminal surface were were injured with the preservation of tight junction and basal lamina. The results indicated that the stress induced acid secretion of parietal cells, which destroys the luminal surface of the epithelium. It thus suggests the significance of epithelial cell membrane damage in the development of stress ulcer.

The aim of the study was to analyze the impact of stress on gastric mucosal hydrophobicity and the dontent of phospholipid in gastric glandular adherent mucus gel layer in rat. Forty rats were randomly divided into four groups, which were control group, 0.5, 1 and 2 h after water immersion restraint stress groups. The gastric mucosal contact angle and the content of phospholipid in mucosal surface scraping material (SSM) of glandualar stomach and gastric mucosal ulcer index were measured. The gastric mucosal contact angle in each group was (38.0?2.4)?、(26 8?1 8)?、(20 0?1 4)? and (14 4?3 3)? respectively. The content of phospholipid in SSM per gram of glandular stomach in each group were (46 76?4 73)、(32 49?9 45)、(25 51?5 78)、(18 14?7 91)、(36 76?4 73)?g respectively and the ulcer index was 0、2.8?1.0、6.0?1.6 and 11.4?3.1 respectively. The three parameters showed significant changes in stress conditions as compared with those in normal control ( P

OBJECTIVE: To compare the therapeutic effects of red peony root decoction, a compound traditional Chinese herbal medicine, and rhubarb in treating severe acute pancreatitis (SAP). METHODS: A total of 96 consecutive patients with objectively-graded SAP were randomly divided into treatment and control groups. There were 48 cases in each group. The patients in the treatment and control groups were assigned to receive red peony root decoction and rhubarb treatment 1-2 times a day via a gastric tube respectively. Comparisons in the time needed for the disappearance of abdominal tenderness, fever and abdominal distension were made between the two groups. The total days of using antibiotics, enzyme inhibitor, protease inhibitor, and nasojejunal feeding start, nasojejunal feeding, gastrointestinal decompression, fasting diet were also compared. And comparison also included hospital stays and hospitalization costs. RESULTS: The durations of abdominal tenderness, fever and abdominal distension in the treatment group were less than those in the control group (P<0.05). Compared with the control group, the time length for antibiotics (including anti-bacteria drug and antifungal agent) use, nasojejunal feeding start, nasojejunal feeding, gastrointestinal decompression, fasting diet, hospital stays and hospitalization costs were decreased in the treatment group (P<0.05). There were no significant differences between the two groups in enzyme inhibitor and protease inhibitor requirement, mortality and adverse reactions. CONCLUSION: Red peony root decoction is more effective than rhubarb alone for SAP patients.

Objective To analyze the etiology in pancreatic pseudocyst (PPC). Methods Medical records were reviewed and analyzed for 366 PPC patients who were admitted in Changhai hospitals from April 2000 to December 2009 in terms. Demographic data, etiology and primary disorders of PPC patients were recorded. Results The causes of 366 patients varied as follow: gallstones in 158 patients (43.2%);idiopathic in 79 (21.6%); alcohol in 50 (13.7%); trauma in 17 (4.6%); pancreatic tumor in 9 (2.5%);hyperlipidemia in 8 (2.2%); post-operative in 7 (1.9%), other in 38 (10.3%). Depending on Atlantes classification systerm the PPCs were classified into acute PPC in 204 patients (64.2%), chronic PPC in 98 patients (30.8%) and abscess in 16 patients (5.0%). The 4 most common causes of acute PPC were gallstones, idiopathic, alcohol and trauma; the 3 most common causes of chronic PPC were gallstones,idiopathic, alcohol. Conclusions Gallstones is the main etiologic cause of the PPCs in China, followed by idiopathic and alcohol, which is significantly different with that in Western countries.

Objective To investigate the effect of apatinib on the proliferation,apoptosis and migration of pancreatic cancer cell line AsPC-1 in vitro.Methods Pancreatic cancer AsPC-1 cells were treated by apatinib in different concentrations.Cell proliferation and apoptosis were measured by CCK-8 and flow cytometry,and the effect of apatinib on cell migration ability was observed by wound healing assay.Results In control and 10,20,30,40 and 50umol/L apatinib treatment group,the inhibitory rates of AsPC-1 cells were 0,(1.45 ±0.68)％,(16.92±0.70)％,(23.84±0.84)％,(34.35±1.55)％ and (37.33± 0.81) ％,respectively.Cell proliferation was obviously inhibited by apatinib as the concentration increased,and the differences were statistically significant (P ＜ 0.05).In control and 20,40 umol/L apatinib treatment group,the apoptotic rates were (9.44 ± 0.18) ％,(16.62 ± 0.19) ％ and (25.42 ± 0.41) ％,respectively.Number of apoptotic cells was obviously increased by apatinib as the concentration increased,and the differences were statistically significant (P ＜ 0.05).In control and 20,40 umol/L apatinib treatment group,the migration ability was (29.5 ± 0.7) ％,(17.4 ± 0.9) ％ and (6.6 ± 0.5) ％,which was greatly decreased as the concentration increased,and the differences were statistically significant (P ＜ 0.05).Conclusions Apatinib can effectively inhibit the proliferation and migration of pancreatic cancer AsPC-1 cells and induce apoptosis.

Objective To observe the changes of zymophagy during experimental acute pancreatitis (AP) induced by caerulein.Methods Pancreatic acinar cell line AR42J cells were cultured in 6-well plates till 90％ confluent and then divided into AP group and control group.Caerulein (1 × 10-8 mol/L) was added into AP group to establish AP cell model,and 1640 cell culture medium was added into control group.After caerulein treated for one,four,six,eight,12 and 24 hours,cells and cell culture supernatant were collected.The levels of cytokine interleukin (IL)-1,tumor necrosis factor (TNF)α,trypsinogen activation (TAP) and amylase were measured with enzyme-linked immunosorbent assay (ELISA) method.The expression of LC3 and Beclin1 at mRNA of each group were detected by reverse transcription-polymerase chain reaction (RT-PCR).The LC3B protein level of each group were detected by Western blotting.The changes of autophagosome and zymophagosome were observed by transmission electron microscopy.The difference between AP group and control group was analyzed by analysis of variance.Results The level of IL-1,TNFα,amylase and TAP in cell culture supernatant of control group was (18.83±7.10) pg/mL,(14.20±3.79) pg/mL,(10.03±2.85) U/L and (39.48±8.62) pg/mL,respectively.Those of AP group significantly increased at first hour ((62.13±11.25) pg/mL,F=3.32,P＜0.01 ; (30.98±7.11) pg/mL,F=3.05,P＜0.05; (25.06±6.82) U/L,F=2.90,P＜0.05 and (128.51± 18.30) pg/mL),F=2.62,P＜0.01,at fourth or sixth hour reached peak (IL-1 at fourth hour:(71.96± 15.82) pg/mL,F=7.25,P＜0.01;TNFα at sixth hour:(39.92±8.94) pg/mL,F=4.93,P＜0.05; amylase at fourth hour:(28.83 ± 8.31) U/L,F=2.06,P＜0.05; TAP at fourth hour:(146.29± 29.36) pg/mL,F=0.14,P＜0.01) and then gradually decreased.At fourth and sixth hour,the expression of LC3 at mRNA level in AP group was 3.18±0.82,1.71±0.14,respectively,while the expression of Beclin-1 rnRNA at first,fourth hour was 2.44±0.34 and 4.13±0.30,all of them were significantly increased compared with those of control group (0.21±0.04 and 0.30±0.08,LC3 mRNA F=0.79、0.06; Beclin mRNA F=2.31、0.36,all P＜ 0.05).There were no significant differences at other time points.The numbers of autophagosome and zymophagosome of AP group were significantly higher than those of control group under transmission electron microscopy.Conclusion Zymophagy occurred during AP cell model induced by caerulein,which suggested that zymophagy might involve in the mechanism of AP.

Background:Damage of intestinal mucosal barrier is a key factor in the development and progress of acute pancreatitis(AP),and is closely related with the prognosis of the disease. Aims:To investigate the protective effect and possible mechanism of mucoprotective agent teprenone on intestinal mucosal barrier in rats with experimental AP. Methods:Forty-five adult male Sprague-Dawley rats were randomly divided into normal control group(n = 5),AP model group(n = 20)and teprenone treated group(n = 20). AP model was established by subcutaneous injection of cerulein at abdominal wall. Rats in treated group were intervened with teprenone intragastrically before and after model establishment. ELISA was used for measurement of serum interleukin-1(IL-1),IL-6,tumor necrosis factor-α(TNF-α)and amylase;histopathological and ultrastructural changes of small intestinal mucosa were observed by light microscope and transmission electron microscope;Western blotting was used to detect the expressions of tight junction protein occludin and ZO-1. Results:Serum levels of IL-1,IL-6,TNF-α and amylase in AP model group were significantly higher than those in normal control group(P < 0. 05),accompanied by necrosis and exfoliation of small intestinal villus,widening of intercellular tight junctions and downregulation of occludin and ZO-1 expression. While in teprenone treated group,serum levels of proinflammatory cytokines and amylase were significantly decreased as compared with AP model group(P < 0. 05),the villus of small intestine remained intact,and dense tight junctions were observed. Expressions of occludin and ZO-1 in teprenone treated group were upregulated. Conclusions:Teprenone may protect against intestinal mucosal barrier injury in AP model rats by upregulating tight junction protein expression.