Abstract: Objective To investigate the reversal effects of tannic acid(TA) on the multidrug resistance of LLC/cMOAT cells and the possible mechanism. Methods MTT assay was used to determine the sensitivity of LLC/CMV and LLC/cMOAT cells to the various kinds of chemotherapeutics,and the activity of LLC/CMV and LLC/cMOAT cells treated with different concentrations of TA. The non-cytotoxic concentrations of TA were determined for the cells and the reversal effects of the chemotherapeutics were observed. The intracellular concent ration of DNR, the cell cycle dist ribution and the apoptosis rate of the cells t reated with different concent rations of TA were determined by flow cytomet ry ( FCM) . Results 　LLC/ cMOAT cells were resistant to CPT-11, ADM, DDP, VCR to a certain extent, and not resistant to VP-16 、TAX. At 10. 0μmol/ L and below, TA was not significantly cytotoxic to LLC/ CMV and LLC/cMOAT cells. TA at the concent ration of 2. 5, 5. 0, 10. 0μmol/ L may remarkably decrease IC50 of LLC/cMOAT cells ( P < 0. 05) . The int racellular DNR fluorescence intensity in LLC/ cMOAT cells was significantly enhanced with the increase of TA concent ration. The cells at G₁ stage increased f rom (46. 35 ± 3. 74) % to (66. 43 ±5. 87) % when t reated with TA at 5. 0μmol/ L for 12 hours. The cell apoptosis was enhanced in a time-and concent ration-dependent manner by t reating with TA. Conclusion 　TA is able to reverse the multidrug resistance of LLC/ cMOAT cells and may remarkably raise drug concent rations in concent ration-dependent manner, TA is able to block cell cycle at G₁ stage, and it s function of inducing apoptosis act s in time-and dose-depended manner. The mechanism may involve the decrease of chemother apeutics excretion, the increase of int racellular drug concent ration, growth arrest at G₁ and apoptosis.