Aim: To investigate the regulatory effects of electroacupuncture (EA) at "Zusanli" (ST 36) on proinflammatory cytokines and myeloperoxidase (MPO) activity in rats with ulcerative colitis (UC), and further elucidate the underlying mechanism of EA on UC. Methods: Thirty-two male SD rats were randomly and evenly divided into four groups: normal control group; UC control group; "Zusanli" (ST 36, EA) group; non-acupoint group. A solution containing ethanol and 2,4,6-trinitrobenzenesulfonate was instilled into the distal colon in the rat (at a dose of 100 mg/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’ treatment, all rats were sacrificed simultaneously. Colon mucosal inflammation and damage were assessed by measuring colon mass, morphologic damage score, colonic MPO activity, contents of serum interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α). Morphologic damage score was examined under stereomicroscope. Colonic MPO was measured by spectrophotometric method. Serum TNF-α,IL-6 and IL-8 were determined by radioimmunoassay (RIA). Results: Both ratio of colonic mass/body mass (mC/mB) and activity of colonic MPO (μkat/g) in rats with UC were markedly increased (P<0.01 vs normal control group). Concentrations of serum TNF-α, IL-6 and IL-8 (ng/L) in rats of UC control group were significantly elevated (P<0.01 vs normal control group). In EA group, mC/mB and activity of MPO were decreased markedly compared with those of UC control group (P<0.05). Serum levels of TNF-α, IL-6 and 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). In comparison with UC control group, no significant changes were observed in the non-acupoint group. Furthermore, there were significant correlations among these parameters. Conclusion: In UC rats, serum TNF-α, IL-6 and IL-8 levels and MPO activity all increase significantly, indicating that these cytokines may cause inflammatory and immune response. EA stimulation induced downregulation on serum TNF-α, IL-6 and IL-8 levels and MPO activity may be responsible for its therapeutic effect in improving UC.
