Purpose: To identify the effects of eleutheroside E (EE) on apoptosis and inflammation induced by doxorubicin (DOX) in H9c2 cells and to investigate the underlying mechanisms. Methods: The effect of EE on H9c2 cell viability was determined using Cell Counting Kit-8 (CCK8). EE effect on DOX-induced apoptosis and inflammation in H9c2 cells was studied by comparison between cells treated with DOX alone and DOX+EE; the relationship between EE effects and NF-kappa B signaling pathway was evaluated by the addition of NF-kappa B inhibitor PDTC. Cell apoptosis was examined by flow cytometry while IL-1 beta, IL-6, and TNF-alpha levels were determined by ELISA. The phosphorylation level of NF-kappa B p65 was measured by Western blot. Results: Compared with control group, cell viability was notably elevated after treatment with 50-100 mu M EE for 48 or 72 h. DOX induced higher rates of cell apoptosis in H9c2 cells (29.5 +/- 3.56 %) compared with control group (6.39 +/- 0.67 %); however, with EE pretreatment (50 and 80 mu M), apoptosis rate decreased to 16.8 +/- 2.16 and 13.54 +/- 2.08 %, respectively, which are significantly lower than that of DOX group; furthermore, the levels of IL-1 beta, IL-6, and TNF-alpha also reduced. In addition, DOX-induced phosphorylation of NF-kappa B p65 was suppressed by EE pretreatment (10, 50 and 80 mu M) to 11.51 +/- 1.25, 40.2 +/- 5.17 and 52.97 +/- 6.74 %, respectively Conclusion: The results suggest that EE treatment reduced DOX-induced apoptosis and inflammation by interacting with NF-kappa B signaling pathway. This finding sheds some light on probable new strategies on the application of DOX for cancer treatment.