0 05). However, the gray of G cells were significantly enhanced( ?

Revised immunoelectron microscopic technique was used to examine G cells and D cells in rat antral mucosa. The number of colloidal gold granules in G and D cells was analysed through quantitative analysis. The results showed that immunological granules of colloidal gold distributed in both G and D cells. Gastrin- or somatostatin-labeled granules were present mainly as lobation-like or island-like congeries. Most of the golden congeries dissociated in the cytoplasm of G or D cells, being in the basement membrane side. A few of the golden congeries located in nucleus. The number of golden granules was 107. 04 ?19. 68 and 83. 36?17. 58 per one G and D cell, respectively.

Objective To investigate the effects of Celecoxib,a selective COX-2 inhibitor,on the healing of gastric ulcer in rats,and reveal the rale of ERK signal transduction pathway in the mechanism of delaying the healing of gastric ulcer.Methods Forty-eight rats were randomly divided into model group(n=40) and sham operation group(n=8).In the rats in model group acetic acid-induced gastric ulcer was reproduced,while in sham operation group,rats underwent the sham procedure.Eight rats in sham-operation group and eight rats in model group were euthanized three days after the procedure.The other thirty-two rats in model group were divided into two subgroups including Celecoxib group and NS group(n=16).Three days after the procedure,rats in Celecoxib group received a gavage of 0.2% Celecoxib solution,and those in NS group received equal amount of 0.9% NaCl solution.Rats in Celecoxib group and NS group were euthanized on sixth and ninth day after ulcer induction(8 rats at each time point in each group).The effects of Celecoxib on the healing of gastric ulcer were observed.Its effects on the activity of Raf-1 and ERK1/2,and the expression level of two transcription factors c-Fos and c-Jun were also determined by Western blot analysis.Results Nine days after ulcer induction,the ulcer area was 11.9?3.1mm2 and 19.7?3.8mm2 in NS group and Celecoxib group,respectively,and they were much smaller than those on third day(P

Isolation of rat gastric mucosal cells was performed with scraping method followed by protease and collagenase digestion. Parietal cells were observed and identified with phase-contrast microscopy, light microscopy with hematoxylin and eosin staining, electron microscopy, fluorescence microscopy, and also immunocytochemistry technique. The diameters of parietal cells were measured. The results showed that the mucosal cells were successfully isolated, and it was confirmed that the parietal cells were the biggest cells among all the mucosal cells.

Objective To study the relationship between gastrointestinal hormones and gastric emptying in functional dyspepsia (FD) patients. Methods Gastric emptying was assessed with solid radiopaque markers in 54 patients with functional dyspepsia, and then all patients were divided into two groups, one with delayed gastric emptying and the other with normal gastric emptying. 17 healthy volunteers served as normal control group. The plasma NT, MTL, Gas and SS levels (fasting and 30 minutes after meal) were measured by radioimmunoassay (RIA). Results The fasting and postprandial plasma NT levels and the postprandial plasma Gas level were significantly higher in FD group with delayed gastric emptying than those in FD group with normal gastric emptying and in normal control group. The MTL levels in fasting and postprandial plasma were significantly lower in FD group with delayed gastric emptying than those in FD group with normal gastric emptying and in normal control group. The plasma SS levels did not show differences among three groups. Conclusion Gastrointestinal dysmyotonia is closely related to NT, MTL and Gas. NT, MTL and Gas may be important in the pathogenesis of FD.

Objective To study the properties of K~ +-ion channel of rat parietal cells, and to approach its effects on physiological and pathological process. Method Parietal cells were isolated. Electrophysiological records of K~ +-ion channels were made through whole cell's patch clamp technique, and the properties of the channels were analyzed. Results 10mM tetraethylammonium chloride may partially block the outwardly depolarized K~ +-ion channel current. While 10mM tetraethylammonium acetate, 10mM barium chloride or 10mM barium acetate may increases the outwardly depolarized K~ +-ion channel current. Conclusion The whole cell K~ +-ion channel current of rat parietal cells showed voltage sensitive. The current-voltage relations of whole cell potassium channels of rat parietal cells are both outwardly and inwardly rectified.

Objective To study the effect of TFF_2 gene theragy on the healing of experimental gastric ulcer in rats and its mechanism.Methods From Jun.10,2005 to Mar.15,2006.48 Wistar rats were randomly divided into two groups:24 in therapy group,24 in control group.pcDNA3.1-TFF_2 100?g was used in each rat in therapy group,and the same volume of pcDNA 3.1 was used in control group.Each rat was injected under serous membrane of the gastric wall after making model.The rats were executed separately after 3、7、14 days.Results Ulcer index was 9.7?2.9 mm2 in therapy group and was 17.7?3.1 mm2 in control group on the 14th day.There was significant difference between the two groups.The average amount of mucous glycoprotein was 83.35?4.54 mg/g in the therapy group and 70.36?4.22 mg/g in the control group.There was no significant change in the secretion of acid between the two groups.Conclusion TFF_2 gene therapy can promote the healing of experimental gastric ulcer in rats.Its mechanisms may include increasing mucous glycoprotein of the gastric wall without suppressing gastric acid secretion.

Objective To study the relationship between gastric emptying dysfunction and neurotensin(NT) in functional dyspepsia(FD) patients. Methods Gastric emptying function in 54 FD patients was measured with solid radioopaque markers. Patients were divided into two groups according to the results, one of which with delayed gastric emptying and the other with normal gastric emptying. Seventeen healthy volunteers served as normal control group. The NT levels in plasma (fasting and postprandial) and the mucosa of gastric antrum and descending portion of duodenum were measured by radioimmunoassay(RIA). Results The NT levels in fasting and postprandial plasma and the mucosa of gastric antrum and descending portion of duodenum in FD group with delayed gastric emptying were significantly higher than those in FD group with normal gastric emptying and in normal control group. The three groups did not differ significantly in incremental extent of plasma NT after test meal. The NT levels in fasting and postprandial plasma and the mucosa of gastric antrum and descending portion of duodenum in FD group with normal gastric emptying did not differ statistically from those in normal control group. Conclusion Gastric emptying dysfunction is closely related to NT, which can inhibit gastrointestinal motility and delay gastric emptying. Thus, NT is important in the pathogenesis of FD.

Objective To investigate the expression changes of histidine decarboxylase(HDC)and H+,K+-ATPase in gastric mucosa during the healing of experimental gastric ulcer in rats.Methods The ulcers were caused by applying acetic acid to the serosal surface of the anterior face of the rat gastric body.At different time points during ulcer healing,HDC and H+,K+-ATPase mRNA and protein expressions were studied by using reverse transcription-polymerase chain reaction and Western blot respectively.Results An ulcer crater developed on the anterior face of the gastric body on day 1 after the induction of ulcers,and the ulcer area was biggest on day 3.On day 12,most of the gastric ulcers had healed.Compared with the control group,the HDC and H+,K+-ATPase mRNA expression in the gastric mucosa of ulcer rats showed a decrease on day 1,and increased back to initial level on day 9.The protein expression of HDC and H+,K+-ATPase in gastric mucosa of ulcer rats decreased immediately on day 1,more on day 6,and returned to the initial levels on day 12.Conclusion The mRNA and protein expressions of HDC and H+,K+-ATPase decrease in the healing process of gastric ulcers,resulting in accelerated ulcer healing through inhibiting gastric acid secretion.

Objective To evaluate the effect of sevoflurane on the expression of aquaporin 8 (AQP8) in the intestinal mucosa in a pig model of hemorrhagic shock.Methods Twenty-four Bama miniature pigs of both sexes, weighing 22-25 kg, were randomly divided into 3 equal groups using a random number table: sham operation group (group S), hemorrhagic shock group (group HS) and sevoflurane group (group PS).The femoral artery and jugular vein were cannulated for blood pressure monitoring, blood-letting, and blood sampling in anesthetized pigs.Hemorrhagic shock was induced by withdrawing blood from the right femoral artery.Hemorrhagic shock was induced after cannulation in group HS.In group PS, 2％ sevoflurane was inhaled for 30 min after the model of hemorrhagic shock was successfully established.Before anesthesia, and at 0.5, 1, 1.5, 2, 3 and 4 h after hemorrhagic shock, blood samples were collected from the jugular vein for determination of serum D-lactic acid and intestinal fatty acid-binding protein (I-FABP) concentrations.The animals were sacrificed at 4 h after hemorrhagic shock, and the intestinal specimens were obtained for microscopic examination and for determination of AQP8 expression in the intestinal mucosa (by enzyme-linked immunosorbent assay).The intestinal water content was calculated.Results Compared with group S, the serum D-lactic acid and I-FABP concentrations, AQP8 expression, and intestinal water content were significantly increased in HS and PS groups (P＜0.05).Compared with group HS, the serum D-lactic acid and I-FABP concentrations, AQP8 expression, and intestinal water content were significantly decreased in group PS (P＜0.05).The pathological changes of intestinal tissues were significantly reduced in group PS as compared with group HS.Conclusion Sevoflurane can decrease the intestinal mucosal edema through inhibiting AQP8 expression, thus reducing hemorrhagic shockinduced damage to the intestinal mucosa in pigs.