To observe the effect of vasoactive intestinal peptide(VIP) or somatostatin (SST) on the lymphocytes traffic in gut-associated lymphoid tissues in rat, 18 rats were divided into three groups at random. VIP and SST were continuously infused from femoral vein at a dose of 60 pmol/h for 7 h. It was found that the lymphocytes in intestinal lymph collected in 5 hours were significantly reduced after VIP and SST administration(P<0.05). Although the volume decreasing of intestinal lymph was happened in all groups, no significant changes in lymph flow were observed in control and treat groups. The percentages of CD8+ cells in intestinal lymph of rat treated by VIP or SST was markedly lower than that in control group (P<0.05). Finally, either VIP or SST infusion reduced CD8+ cells in the small intestinal mucosa when compared with control. It concludes that either VIP or SST not only reduces lymphocytes, especially CD8+ cells traffic from intestinal mucosa immune system to other organs and systemic immune system but also suppresses the homing of CD8+lymphocytes into intestinal mucosa immune system in rats.

Objective: To observe the effect of VIP or SST on the lymphocyte homing to the intestinal tract. Methods: Intestinal lymph were collected from mesenteric lymphatic duct of rats. Intestinal lymphocytes, which had been incubated with VIP or SST, were labeled with 51Cr and then were infused into blood circulation of rats. The 51Cr-intestinal lymphocytes in organs (or tissues)were determined with γ-counter. Results: About 10% of 51Cr-intestinal lymphocytes homed to intestinal tract within 1 h at normal physiological state. The distribution of 51Cr-intestinal lymphocytes treated with either VIP or SST in mesenteric node (1.83% or1.56%) and in Peyer's patches (1.85% or 1.60%) were significantly lower than that of control group (3.83%, 3.85%), P<0.05. VIP or SST did not show remarkable affection on the homing of 51Cr-intestinal lymphocytes to diffusive lymphatic tissue in small intestine when compared with control. Conclusion: Either VIP or SST reduces the homing of intestinal lymphocytes to mesenteric nodes and Peyer's patches in rats.

[Abstract]: Multiple organ failure (MOF) is the most serious result followed by trauma and infection. Our previous study has shown that activated intestinal mucosal mast cells (IMMC) may play an important role in the development of MOF. Somatostatin (SST), one of gut peptides, is an important regulator in the neuro-endocrine-immune network. However, the effects of SST on IMMC especially in the case of MOF remain unclear. Objective: This study was aimed to investigate the effect of SST on the activity of IMMC in the development of MOF. Methods: The rat model of MOF was established by injection of zymosan. Thirty minutes after the injection of zymosan, SST at 2.3ng/Kg/h or 0.023ng/Kg/h was injected respectively through tail veins. The concentration of histamine and tumor necrosis factor-α (TNF-α) in plasma and intestine tissue were measured. The pathological alterations of essential organ including intestine, liver, kidney and lung were studied under light microscope. Their corresponding functions were reflected with alanine aminotransferase (ALT), cretinine (Cr) and oxygen pressure (PO2). In addition, the ultra structure of the IMMC was observed under a transmission electronic microscope. Results: Compared with the controlled rats, the rats injected with SST (2.3ng/Kg/h) showed less serious inflammatory response under light microscope. ALT and Cr were decreased 53% and 60% respectively. However, PO2 was increased 50%. The histamine level in the intestinal tissue from rats treated with SST remarkably increased (8.60±0.50 to 14.50±1.08 ng/g protein), while the plasma histamine level did not show any significant changes. Exdogeneous SST also resulted in lower level of TNF-α in intestine but no changes in plasma. Furthermore, degranulation of IMMC from the rats treated with SST was less obvious. Conclusions: SST may prevent from or arrest the development of MOF through suppression of inflammatory mediators releasing such as histamine and TNF-α.

Objectives: Somatostatin and its analogues may suppress the growth of various tumor cells. However, the effect of octreotide on growth of gastric adenocarcinoma is still largely unknown. This study was to explore if octreotide could inhibit the growth of gastric adenocarcinoma and the probable mechanisms behind the effects. Methods: Proliferation of gastric cancer cell line affected with octreotide was determined by 3H-thymidine incorporation. After xenografts of human gastric cancer were implanted orthotopically in stomach, nude mice were administrated octreotide for 8 weeks. The mRNA of somatostatin receptor in the SGC-7901 cells was detected by reverse transcription polymerase chain reaction technique. Extrcellular signal-regulated protein kinase and c-Fos in gastric cancer tissues were measured by immunohistochemistry and western blot. Activator protein-1 binding activity was examined by electrophoretic mobility sift assay. Results: 3H-thymidine incorporation into SGC-7901 cells was significantly decreased by octreotide in a manner of concentration dependence. Either size or weight of tumors treated with octreotide was significantly reduced in vivo. The inhibition rate for tumor was 62.3% in octreotide group. The genes of somatostatin receptor 2 and 3 were expressed in SGC-7901 gastric cancer cell lines. Extracellular signal-regulated protein kinase and the c-Fos protein level were decreased in gastric adenocarcinoma treated with octreotide. Moreover, the fetal calf serum stimulated activator protein-1 binding activity could be suppressed by octreotide potentially. Conclusions: Inhibition of sequential molecular events in MAPK pathway may interpret the mechanisms behind the suppressive effect of octreotide on the growth of gastric adenocarcinoma.

Objective: To study the effect of somatostatin analogue octreotide on the invasion and metastasis of gastric cancer in vitro and in vivo. Methods: Using membrane invasion culture system alone or coated with matrigel, we observed the effect of octreotide on blocking migration and invasion of gastric carcinoma cells. Nude mice implanted orthotopically with SGC-7901 human stomach carcinoma were given injections of octreotide for 8 weeks. MMP-2 was detected by gelatin zymography or RT-PCR. The microvascular density and VEGF expression were examined by immunohistochemical staining with factor VIII antibody and VEGF antibody. Results: Octreotide significantly inhibit migration(49.8