Basic Research
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 15, 2003; 9(5): 1028-1033
Published online May 15, 2003. doi: 10.3748/wjg.v9.i5.1028
Downregulation of electroacupuncture at ST36 on TNF-α in rats with ulcerative colitis
Li Tian, Yu-Xin Huang, Min Tian, Wei Gao, Qing Chang
Li Tian, Yu-Xin Huang, Wei Gao, Qing Chang, Department of Gastroenterology, Tangdu Hospital, Fourth Military Medical University, Xi’an 710038, Shaanxi Province, China
Min Tian, Department of Ultrasound, Heping Hospital of Changzhi Medical College, Changzhi 046000, Shanxi Province, China
Author contributions: All authors contributed equally to the work.
Supported by the National Nature Science Foundation of China, No. 39970888
Correspondence to: Dr Yu-Xin Huang, Department of Gastroenterology, Tangdu Hospital, 4th Military Medical University, Xi’an 710038, Shaanxi Province, China.
Telephone: +86-29-3577597
Received: November 12, 2002
Revised: November 23, 2002
Accepted: December 30, 2002
Published online: May 15, 2003

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 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 control group, 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 the distal colon in the rat (at a dose of 100 mg/kg) to set up UC rat model. Rats in wakefulness state of UC+ST36 group were stimulated at ST36 by EA once a day, while those of UC+non-acupoint group were done at 0.5 cm beside ST36. After 10 d treatment, all rats were sacrificed simultaneously. Colon musocal inflammation and damage were assessed by measuring colon mass, morphologic damage score, colonic myeloperoxidase enzyme (MPO) activity, serum TNF-α and colonic TNF-α mRNA level. Morphologic damage score was examined under stereomicroscope. Colonic 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 mass (mC/mB) and activity 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 normal control group). Compared with normal control rats, serum TNF-α and colonic TNF-α mRNA level in UC control group were increased 2.5 fold (2278 ± 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, mC/mB and MPO activity were reduced significantly (5.3 ± 2.0 vs 8.5 ± 2.6; 104 ± 36 vs 145 ± 25, P < 0.01, 0.05) compared with those of UC control group. Serum TNF-α and colonic TNF-α mRNA level were inhibited by EA stimulation at ST36 (P < 0.01). The inhibitory rate was 16% and 44% respectively. Morphologic damage score was also increased markedly in rat with UC (P < 0.01), whereas it was decreased by EA at ST36 (P < 0.05). There was no significant difference between UC control group and UC+EA at non-acupoint (P > 0.05). Furthermore, these parameters were highly correlated with each other (P < 0.01).

CONCLUSION: Serum TNF-α concentration and colonic TNF-α mRNA expression level are increased significantly in UC rats in correlation with the severity of disease. It indicates that TNF-α is closely involved in the immune abnormalities and inflammatory responses in UC. EA at ST36 has therapeutic 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 implicated in the pathogenesis of UC.

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