In this study, in vitro cytotoxicity of carboxymethyl chitosan-rhein conjugate(CR conjugate)and paclitaxel-loaded carboxymethyl chitosan-rhein polymeric micelles(PTX/CR PMs)was evaluated by MTT method in MCF-7 cells. The results showed that CR conjugate displayed good security; PTX/CR PMs in 24 h showed better antitumor activity than Taxol® . Environment-responsive fluorescent probe P4 was used to determine the cellular uptake of PTX/CR PMs in MCF-7 cells. The results also showed that P4 and PTX co-loaded carboxymethyl chitosan-rhein polymeric micelles ［(P4+PTX)/CR PMs］ could be taken up by MCF-7 cells. There was no difference between(P4+PTX)/CR PMs group and(P4+PTX)/CR PMs with verapamil group, suggesting that CR PMs could protect fluorescent probe and/or drugs in their cores avoiding efflux by P-glycoprotein. These results will contribute to in vivo study of CR conjugate and PTX/CR PMs in the future.

To study the inhibitory effect of celastrol respectively combined with glycyrrhetic acid, paclitaxel, and rhein on the proliferation of human hepatoma cell line HepG2. The MTT method was used to detect the survival rate of HepG2 cells. The cooperativity index(CI)and Jin′s formula method were used to determine the synergistic effect. Apoptosis and cell cycle arrest were detected, too. The results show that celastrol, glycyrrhetinic acid, rhein, and paclitaxel alone can inhibit the proliferation of HepG2 cells, respectively. Combination with glycyrrhetic acid, paclitaxel, and rhein, respectively, the inhibitory effect of celastrol on the proliferation of HepG2 cells was significantly enhanced. And the synergistic effect on the proliferation inhibition of HepG2 cells in some concentrations was displayed in the experiment. The cell apoptosis rate was improved(P< 0. 01)and more cells were arrested in G2/M phase. Celastrol respectively combined with glycyrrhetic acid, paclitaxel, and rhein displayed a synergistic inhibitory effect on the proliferation of HepG2 cells, and the effect was related to inducing cell apoptosis and increasing the cell cycle arrest in G2/M phase.