| To use human erythroleukemia drug resistant cell line K562/A02 as an experimental model, to research the effect of TSPG on the drug resistance of K562/A02 cell line and its mechanism.Methods: The sensitivity of untreated and TSPG-treated K562/A02 cells to anticancer drugs was determined by MTT assay. Immunohistochemistry method was used to measure mdr-1 gene product P-gp and bcl-2 protein expression. RT-PCR technique was used to examine mdr-1 mRNA expression.Results: (1) TSPG inhibition of K562/A02 cells was in direct proportion to TSPG concentration: inhibition percentages for TSPG concentrations of 50μg/ml, 100μg/ml, 150μg/ml, and 200μg/ml were 0, 0.28%, 2.83%, and 13.31%, respectively. Concentrations of less than 200μg/ml were regarded to be non-toxic dosage. (2) In non-toxic dosages, TSPG strengthened the toxicity effect of Doxorubicin on K562/A02 cells. The 50% inhibitory concentration, (IC50, μg/ml) for the K562/A02 control group, the TSPG50μg/ml group, the TSPG100μg/ml group, and the TSPG150μg/ml group, were 5.980, 4.138, 3.248, and 1.281, respectively. The ratios of the TSPG group IC50s to the control group were 1.45, 1.84, and 4.67, respectively, and the relative reverse ratios were 31.43%, 46.63%, and 80.19%. These results implied that the reversing effect of TSPG on drug resistance of K562/A02 cells to Doxorubicin was related to its concentration. The drug resistance multiple of K562/A02 cells was 49.83. (3) Decrease in P-gp expression in K562/A02 cells was marked (P<0.01) after 3 days of TSPG(150μg/ml) application to K562/A02 cells. (4) The change in bcl-2 protein expression was insignificant (P>0.05) after 3 days of TSPG(150μg/ml) treatment. (5) Decrease in mdr-1 mRNA expression was significant (P<0.01) after 24 hours of TSPG(150μg/ml) treatment.Conclusions: (1) Non-toxic dosages of TSPG partly reverse the drug resistance of K562/A02 cells, and the effect is directly proportional to the concentration. (2) The main mechanism by which TSPG reverses the drug resistance of K562/A02 cells is by decreasing the expression of mdr-1 mRNA, which then decreases P-gp, the product of mdr-1 mRNA. This leads to an accumulation of anticancer drug in cancer cells, which strengthens toxicity. (3) The relationship between bcl-2 protein expression and the mechanism by which TSPG reverses the drug resistance of K562/A02 cells is not clear. |