Eleutheroside E inhibits doxorubicin-induced inflammation and apoptosis in rat cardiomyocytes by modulating activation of NF-κB pathway

  • Zheng Wu
  • Wenzheng Li
  • Yuhua Sun
  • Kun Fu
  • Shujuan Cheng
Keywords: Eleutheroside E, Doxorubicin, Inflammation, Apoptosis, Cardiomyocytes, NF-κB


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-κB signaling pathway was evaluated by the addition of NF-κB inhibitor PDTC. Cell apoptosis was examined by flow cytometry while IL-1β, IL-6, and TNF-α levels were determined by ELISA. The phosphorylation level of NF-κB p65 was measured by Western blot.
Results: Compared with control group, cell viability was notably elevated after  treatment with 50-100 μM 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 μM), 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-1β, IL-6, and TNF-α also reduced. In addition, DOX-induced phosphorylation of NF-κB p65 was suppressed by EE pretreatment (10, 50 and 80 μM) 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-κB signaling pathway. This finding sheds some light on probable new strategies on the application of DOX for cancer treatment.

Keywords: Eleutheroside E, Doxorubicin, Inflammation, Apoptosis, Cardiomyocytes, NF-κB


Journal Identifiers

eISSN: 1596-9827
print ISSN: 1596-5996