Key Word(s): 1. diagnosis; 2. T-SPOT. TB; 3. γ-interferon; 4. peritonitis; Presenting Author: CHONG WANG Additional Authors: YUAN-YUAN LI, JUAN WAN, LE-YING YANG, GUO-HUA LI Corresponding Author: GUO-HUA LI Affiliations: The First Affiliated Hospital of Nanchang University Objective: The aim was to investigate ABT-737 cell line the influence of vasoactive intestinal peptide (VIP) and its antagonist on cytotoxic effect of NK cell to killing gastric cancer cells in vitro, and the

relationship of this influence with NKG2D, DAP10 and NF-κB signal molecules in NK cells. Methods: NK cells was isolated and purified from peripheral blood mononuclear cells (PBMC). The expressions of VIP, VIPR were detected in NK cells and MKN45 cells. Before and after NK cells were incubated with VIP in 10–5 to 10–7 mol/L concentration and/or its antagonist (D-p-Cl-Phe6, Leu17)-VIP in 10–4 to 10–6 mol/L concentration for 24 h, 48 h,

and 72 h receptively, we detected the cytotoxic effect of NK cells to kill MKN45 gastric cancer cells by MTT, and detected the expressions of NKG2D, DAP10 and NF-κB proteins and mRNAs in NK cells by immunocytochemistry and RT-PCR. Then we analyzed the effect of VIP on expressions of NKG2D, DAP10 and NF-κB signal molecules in NK cells, and on the cytotoxic effect of NK cells to MNK45 gastric cancer cells. Results: NK cells were purified by CDC method was highly enough to satisfy the experiment needs (60.583%). The expression of VIP mRNA and protein did not find in NK cells and MKN45 cells. However, VPAC1 could be detected in them. Exogenous VIP and its antagonist did not affect the proliferation of MKN45 Carfilzomib in vivo cells. VIP could inhibit the cytotoxic effect of NK cells to MKN45 cells (P < 0.05), and could inhibit the expressions of this website NKG2D, DAP10 and NF-κB in NK cells. However, (D-p-Cl-Phe6, Leu17)-VIP could reverse those effects.

Conclusion: The inhibiting influence of VIP on the cytotoxic effect of NK cell to MKN45 cells might get through inhibiting the expressions of NKG2D signal molecules in NK cells. This may be one mechanism of gastric cancer cells escaping organism immune clearing. Key Word(s): 1. VIP; 2. NKG2D; 3. DAP10; 4. MKN45; Presenting Author: LE-YING YANG Additional Authors: BO GAN, FENG-LI WU, GUAN GUI, PENG YE, GUO-HUA LI Corresponding Author: GUO-HUA LI Affiliations: the First Affiliated Hospital of Nanchang University Objective: To observe the expressions of SIRPα1 (signal regulatory protein α, SIRPα1), CD68(the marker of macrophage), IL-10 and IL-12 proteins in the inflammatory cells of gastric carcinoma tissue and normal gastric tissue beside carcinoma, and evaluate the relations between SIRPα1 proteins in the inflammatory cells and the M2-polarized tumor-associated macrophages. Methods: A database including 58 patients who received a gastric cancer surgery at the First Affiliated Hospital of Nanchang University from April 2011 to November 2011 were compiled and analyzed in this study.