Abstract: Objective To establish an experimental model of lipopolysaccharide (LPS)-induced degranulation ofPaneth cells, and to investigate the role of NF-kB pathway and its possible mechanism.Methods Eighteen male KM mice were randomly divided into control, LPS and PDTC groups. In each group, the small intestines were intubated. The control group were perfused with physiological saline.The experimental groups were perfused with LPS (100 jog/ml, 1.5 ml/h)and were injected intraperito-neally with saline or NF-kB inhibitor PDTC one hour before surgery. Then the perfusates were collected in three periods (0～30 min, 30-60 min，60-120 min). Lysozyme concentration in perfusates were tested by ELISA. The relative concentrations were expressed as the ratio of lysozyme concentration to basal levels. NF-kB activity in intestinal mucosa was observed by immunohistochemistry. Results ① Relative concentration of lysozyme in LPS group was significantly higher than that in control group at all time duration (P<0.05). (2) Relative concentration of lysozyme in PDTC group was lower than that in LPS group. The difference in 60～120 min was statistically significant (P<0.05). (3) Immunohistochemistry showed that，in LPS group, strong positive staining of NF-kB p65 was observed in the cytoplasm and (or) nuclei, including epithelial cells in the middle and upper crypts, villous epithelial cells and lamina propria cells. Weak positive staining was observed only in Paneth cells. The staining intensity of the PDTC group were significantly weaker than that in other groups. Conclusion LPS can induce Paneth cell degranulation. NF-icB signaling pathway may be involved in this process. NF-icB signaling pathway may act as an indirect way, i.e. LPS first activates the cells beyond the crypt bottom through the NF-icB pathway, then leads to Paneth cell degranulation by yet unknown mechanisms.

Key words: Paneth cell, NF-kB, Lipopolysaccharide, Degranulation, Pattern recognition receptor