Objective To study the effects of wedelolactone on the expression of P-glycoprotein (P-gp) and to explore the multi-drug resistance reversing mechanism of wedelolactone in K562/A02 cells in vitro.Methods The half maximal inhibitory concentration of ADM in K562/A02 was determined by MTT method.The protein expression level of P-gp was determined by Western blot after wedelolactone pretreatment.Results Wedelolactone remarkably enhanced chemo-sensitivity to ADM of K562/A02 cells.After 0.2, 2, 20 μmol/L different concentration of wedelolactone treatment in 24 h, the relative reversal efficiency of K562/A02 to ADM was 23.5％, 47.1％ and 67.7％, respectively.according to the results of Western blot, wedelolactone was shown to efficiently inhibit the expression of P-gp (P＜0.05).The relative efficiency of K562/A02 to ADM was 25.4％,46％ and 55.6％, respectively.Conclusion Wedelolactone could modulate P-gp expression, and P-gp expression down regulation may be one of the MDR reversal mechanisms in K562/A02 cells by wedelolactone.

Objective To investigate the effect of clotrimazole on apoptosis of hepatic cells after ischemia-reperfusion injury and its mechanism. Methods Hepatic ischemia-reperfusion rat model was established. Thirty-two male Sprague-Dawley rats were randomly allocated into sham-operated group, model control group, low dose clotrimazole group and high dose clotrimazole group. Apoptosis in hepatic tissue was assessed by TUNEL method. Protein expression levels of CYP3A1,Bcl-2,Bax and PARP were measured by Western blotting. Results As compared with model control group, the apoptosis rate, tissue injury,activity of plasma enzymes and the Bax/Bcl-2 expression ratio were reduced in low and high dose clotrimazole groups. The apoptotic index in both clotrimazole-treated groups was lower than that of model control group with statistically significant difference. CYP3A1 expression was significantly induced by clotrimazole compared to the sham-operated group. Conclusion Clotrimazole may inhibit apoptosis of hepatic cells by up-regulating Bcl-2 and down-regulating Bax, thus produce a protective effect on hepatic ischemia-reperfusion injury and it is also related to the inhibition of PARP shear.