Objective: To investigate the protective effect of anti-TNF-α monoclonal antibody (anti-TNF-α) against the myocardial impairment induced by acute obstructive jaundice. Methods: Twenty-four male SD rats were equally randomized into the model group (undergoing common bile duct ligation), anti-TNF-α treatment group (with administration of anti-TNF-α after common bile duct ligation) and sham operation group. The rats of the anti-TNF-α treatment group were injected with anti- TNF-α (1 mg/kg) through tail vein from the third postoperative day for 5 consecutive days, and those of the model group and sham operation group were given the same volume of saline under the same administration regimen. On the seventh postoperative day, the serum level of creatine kinase (CK-MB) and TNF-α, the malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in myocardial tissues of the rats were detected; the morphological changes in the myocardial tissues of the rats were also assessed. Results: Except for the sham operation group, rats in both the model group and anti-TNF-α treatment group began to present jaundice that gradually increased. The serum CK-MB and TNF-α levels and the myocardial MDA contents were significantly increased, and the myocardial SOD activities were significantly decreased on the seventh postoperative day in both the model group and anti-TNF-α treatment group compared with the sham operation group (all P<0.01). However, the changes of above indexes in the anti-TNF-α treatment group were less evident than those in the model group and all the differences had statistical significance (all P<0.01). The myocardium from the sham operation group had no obvious pathological change under the light microscope, while the rats of the model group showed sparse atrophied cardiac muscle fibers with necrosis and cloudy swelling, and the pathological changes of myocardial impairment was relatively mild in anti-TNF-α treatment group. Conclusion: TNF-α may be an important mediator in myocardial injury following acute obstructive jaundice, and anti-TNF-α can lessen the myocardial injury by antagonizing the action of TNF-α.