AIM:To investigate the protective effect of ketamine onthe endotoxin-induced proinflammatory cytokines and NF-kappa B activation in the intestine.METHODS:Adult male Wistar rats were randomly dividedinto 6 groups:(a) normal saline control,(b) challenged withendotoxin (5 mg/kg) and treated by saline,(c) challenged withendotoxin (5 mg/kg) and treated by ketamine (0.5 mg/kg),(d) challenged with endotoxin (5 mg/kg) and treated byketamine (5 mg/kg),(e) challenged with endotoxin (5 mg/kg)and treated by ketamine (50 mg/kg),and (f) saline injectedand treated by ketamine (50 mg/kg).After 1,4 or 6 h,TNF-αand IL-6 mRNA were investigated in the tissues of the intestine(jejunum) by RT-PCR.TNF-α and IL-6 were measured byELISA.We used electrophoretic mobility shift assay (EMSA)to investigate NF-kappa B activity in the intestine.RESULTS:NF-kappa B activity,the expression of TNF-αand IL-6 were enhanced in the intestine by endotoxin.Ketamine at a dose of 0.5 mg/kg could suppress endotoxin-induced TNF-α mRNA and protein elevation and inhibit NF-kappa B activation in the intestine.However the least dosageof ketamine to inhibit IL-6 was 5 mg/kg in our experiment.CONCLUSION:Ketamine can suppress endotoxin-inducedproduction of proinflammatory cytokines such as TNF-α andIL-6 production in the intestine.This suppressive effect mayact through inhibiting NF-kappa B. AIM: To investigate the protective effect of ketamine on the endotoxin-induced proinflammatory cytokines and NF-kappa B activation in the intestine. METHODS: Adult male Wistar rats were randomly divided into 6 groups: (a) normal saline control, (b) challenged withendotoxin Challenged with endotoxin (5 mg / kg) and treated by ketamine (5 mg / kg), and treated by saline (c) challenged withendotoxin (50 mg / kg) .After 1, 4 or 6 h (5 mg / kg) and treated by ketamine (50 mg / kg) , TNF- [alpha] and IL-6 mRNA were investigated in the tissues of the intestine (jejunum) by RT-PCR. TNF- [alpha] and IL-6 were measured by ELISA. We used electrophoretic mobility shift assay (EMSA) to investigate NF- kappa B activity in the intestine. RESULTS: NF-kappa B activity, the expression of TNF-αand IL-6 were enhanced in the intestine by endotoxin. Ketamine at a dose of 0.5 mg / kg could suppress endotoxin- induced TNF- α mRNA and protein elevation and inhibit NF-kappa B activation in the intestine. Although the least dosage of ketamine to inhibit IL-6 was 5 mg / kg in our experiment. CONCLUSION: Ketamine can suppress endotoxin-induced production of proinflammatory cytokines such as TNF- α and IL-6 production in the intestine. This suppressive effect may act through inhibiting NF-kappa B.