AIM:To investigate the regulatory effect of electroacupuncture(EA) at Zusanli (ST36) on tumor necrosis factor-alpha (TNF-α) in rats with ulcerative colitis (UC),and further elucidatethe therapeutic mechanism of EA on UC.METHODS:Thirty-two male Sprague-Dawley (SD) rats wererandomly divided into four groups (n=8):normal controlgroup,UC control group,UC+ST36 group and UC+non-acupoint group.A solution containing ethanol and 2,4,6-trinitrobenzenesulfonic acid (TNBS) was instilled into thedistal colon in the rat (at a dose of 100 mg/kg) to set up UCrat model.Rats in wakefulness state of UC+ST36 group werestimulated at ST36 by EA once a day,while those of UC+non-acupoint group were done at 0.5 cm beside ST36.After 10d treatment,all rats were sacrificed simultaneously.Colonmusocal inflammation and damage were assessed bymeasuring colon mass,morphologic damage score,colonicmyeloperoxidase enzyme (MPO) activity,serum TNF-α andcolonic TNF-α mRNA level.Morphologic damage score wasexamined under stereomicroscope.Colonic MPO activity wasmeasured by spectrophotometer method.Serum TNF-αconcentration was determined by radioimmunoassay (RIA).Colonic TNF-α mRNA expression level was analyzed bysemiquantitative reverse transcription polymerase chainreaction (RT-PCR).RESULTS:Ratio of colonic mass/body mass (m_C/m_B) andactivity of colonic MPO (μkat/g tissue) markedly increased(8.5±2.6 vs 2.5±0.4;145±25 vs 24±8,P<0.01 vs normalcontrol group).Compared with normal control rats,serumTNF-α and colonic TNF-α mRNA level in UC control groupwere increased 2.5 fold (2 278±170 vs 894±248,P<0.01)and 4.3 fold (0.98±0.11 vs 0.23±0.11,P<0.01)respectively.After EA at ST36,m_C/m_B and MPO activitywere reduced significantly (5.3±2.0 vs 8.5±2.6;104±36 vs145±25,P<0.01,0.05) compared with those of UC controlgroup.Serum TNF-α and colonic TNF-α mRNA level wereinhibited by EA stimulation at ST36 (P<0.01).Theinhibitory rate was 16% and 44% respectively.Morphologic damage score was also increased markedlyin rat with UC (P<0.01),whereas it was decreased by EAat ST36 (P<0.05).There was no significant differencebetween UC control group and UC+EA at non-acupoint (P>0.05).Furthermore,these parameters were highlycorrelated with each other (P<0.01).CONCLUSION:Serum TNF-α concentration and colonicTNF-α mRNA expression level are increased significantly inUC rats in correlation with the severity of disease.It indicatesthat TNF-α is closely involved in the immune abnormalitiesand inflammatory responses in UC.EA at ST36 hastherapeutic effect on UC by downregulating serum TNF-αand colonic TNF-α mRNA expression.High levels of TNF-αand its corresponding mRNA expression seem to beimplicated in the pathogenesis of UC. To investigate the regulatory effect of electroacupuncture (EA) at Zusanli (ST36) on tumor necrosis factor-alpha (TNF-a) in rats with ulcerative colitis (UC), and further elucidate the therapeutic mechanism of EA on UC. METHODS: Thirty -two male Sprague-Dawley (SD) rats were randomly divided into four groups (n = 8): normal controlgroup, UC control group, UC + ST36 group and UC + non-acupoint group. -trinitrobenzenesulfonic acid (TNBS) was instilled into the distal colon in the rat (at a dose of 100 mg / kg) to set up UCrat model. Rats in wakefulness state of UC + ST36 group werestimulated at ST36 by EA once a day, while of UC + non-acupoint group were done at 0.5 cm beside ST36. After 10d treatment, all rats were sacrificed simultaneously.Colonmusocal inflammation and damage were assessed bymeasuring colon mass, morphologic damage score, colonic myeloperoxidase enzyme (MPO) activity, serum TNF- α andcolonic TNF-α mRNA level. Morphological damage score wasexamined under stereomicroscope. Colo MPO activity was measured by spectrophotometer method. Serum TNF-α concentration was determined by radioimmunoassay (RIA). Colonic TNF-α mRNA expression level was analyzed by semiquantitative reverse transcription polymerase chain reaction (RT-PCR) .RESULTS: Ratio of colonic mass / body (8.5 ± 2.6 vs. 2.5 ± 0.4; 145 ± 25 vs 24 ± 8, P <0.01 vs. normal control group) .Compared with normal control rats, serum TNFα (μ kat / g tissue) α and colonic TNF-α mRNA levels in UC control groupwere increased by 2.5 fold (2 278 ± 170 vs 894 ± 248, P <0.01) and 4.3 fold (0.98 ± 0.11 vs 0.23 ± 0.11, P <0.01) at ST36, m_C / m_B and MPO activitywere reduced significantly (5.3 ± 2.0 vs 8.5 ± 2.6; 104 ± 36 vs 145 ± 25, P <0.01, 0.05) compared to those of UC control group. level were inhibited by EA stimulation at ST36 (P <0.01). The inhibition rate was 16% and 44% respectively. Morphologic damage score was also incr eased markedlyin ratwith no UC (p & lt; 0.01), with it UC decreased by EAat ST36 (P <0.05). There was no significant difference between UC control group and UC + EA at non-acupoint each other (P <0.01) .CONCLUSION: Serum TNF-α concentration and colonic TNF-α mRNA expression level are significantly increased in in rats in correlation with the severity of disease. It indicatesthat TNF-α is closely involved in the immune abnormalities and inflammatory responses in UC. EA at ST36 hastherapeutic effect on UC by downregulating serum TNF-α and colonic TNF-α mRNA expression. High levels of TNF-α and its corresponding mRNA expression seem to be disseminated in the pathogenesis of UC.