Effects of Rh-endostatin (YH-16) on the proliferation of murine hemangioendothelioma cell line EOMA

Objective To investigate the mechanism of inhibitory effects of rh-endostatin (YH16,endostar) on the proliferation of murine hemangioendothelioma cell line(EOMA) in vitro,compare its inhibitory effects with Triamcinolone Acetonide,Pingyangmycin (PYM),interferon alpha 2a,and observe the combined inhibitory effects on the growth of EOMA cells in vitro.Methods The IR of EOMA cells managed by different concentration of YH-16 for 24 h,48 h and 72 h were compared by MTT assay to get an optimal concentration.MTT assay was also used to detect the combined effect of any two of YH-16,Triamcinolone Acetonide or PYM.The changes of apoptosis and Caspase-3 protein expression were examined by flow cytometry (FCM) after YH-16 treatment for 48 h.Results YH-16 with different concentration had significant inhibitory effect on proliferation of EOMA cells at 24 h,48 h and 72 h(P＜0.01),and IR and the concentration had significant dose-effect relationship.The optimal concentration of YH-16 was 200 μg/ml.The inhibitory effects from the strongest to the weakest was as follows:PYM＞YH-16＞Triamcinolone Acetonide＞interferon alpha 2a.Q value of YH-16 combined with Triamcinolone Acetonide or PYM was lower than 0.85,but Q value of Triamcinolone Acetonide combined with PYM was between 0.85 and 1.15.The apoptosis rate of EOMA cells treated with YH-16 for 48h was also concentration-dependant.The expression of Caspase 3 increased in all groups with different concentration (P＜0.01 ).Conclusions YH-16 can effectively inhibit the growth of EOMA cells.Its inhibitory effect is stronger than that in Triamcinolone Acetonide and interferon alpha 2a,but weaker than PYM.The inhibitory mechanism of YH-16 is to induce apoptosis with the participation of Caspase-3.YH-16 can be an antagonism to Triamcinolone Acetonide and PYMs in the inhibition of FOMA proliferation,and the combination of Triamcinolone Acetonide and PYM has an effect of addition. Key words: Hemangioma; Endostatins; Endothelial cells; Drug synergism