Aim: To investigate the regulatory effects of electroacupuncture (EA) at "Zusanli" (ST 36) on proin-flammatory cytokines and myeloperoxidase (MPO) activity in rats with ulcerative colitis (UC), and further elucidate theunderlying mechanism of EA on UC. Methods: Thirty-two male SD rats were randomly and evenly divided into fourgroups: normal control group; UC control group; "Zusanli" (ST 36, EA) group; non-acupoint group. A solution con-taining ethanol and 2,4,6-trinitrobenzenesulfonate was instilled into the distal colon in the rat (at a dose of 100 rng/kg)to set up UC model. Non-anesthetized rats of EA group were stimulated at ST-36 by electroacupuncture once a day,while those of non-acupoint group were done at the site 0.5 cm beside ST-36. After 10 days' treatrment, all rats weresacrificed simultaneously. Colon mucosal inflammation and damage were assessed by measuring colon mass, morpho-logic damage score, colonic MPO activity, contents of serum interleukin-6 (IL-6), interleukin-8 (IL-8) and tumornecrosis factor-alpha (TNF-α). Morphologic damage score was examined under stereomicroscope. Colonic MPO wasmeasured by spectrophotometric method. Sertm TNF-α, IL-6 end IL-8 were determined by radioimmunoassay (RIA).Results: Both ratio of colonic mass/body mass (mC/mB) and activity of colonic MPO (iμkat/g) in rats with UC weremarkedly increased (P＜ 0.01 vs normal control group). Concentrations of sertrn TNF-a, IL-6 and IL-8 (ng/L) in ratsof UC control group were significantly elevated (P＜0.01 vs normal control group). In EA group, mC/mB and activityof MPO were decreased markedly compared with those of UC control group (P＜0.05). Serum levels of TNF-α, IL-6end IL-8 of ST-36 group were decreased by EA of ST-36 (P＜0.01; P＜0.05; P＜0.05 vs UC control group). Incomparison with UC control group, no significant changes were observed in the non-acupoint group. Furtherrnore, therewere significant correlations among these parameters. Conclusion: In UC rats, sertum TNF-a, IL-6 and IL-8 levels andMPO activity all increase significantly, indicating that these cytokines may cause inflammatory and immune response.EA stimulation induced downregulation on serum TNF-a, IL-6 and IL-8 levels and MPO activity may be responsible forits therapeutic effect in improving UC.