3.5 LCZ696 treatment and TLR2 knockdown attenuated the doxorubicin-induced H9C2 cell inflammatory response in vitro.
Furthermore, we also assessed the inflammatory response induced by DOXin vitro . Similar to the above results, TLR2 silencing completely reversed DOX-induced IκB-a degradation and the nuclear translocation of NF-κB (Figure 5A-D). In addition, cardiac inflammation was ameliorated by TLR2 knockdown, as shown by the gene expression of Tnfa, Mcp1, and Il-6 (Figure 5E-G).
These results provide evidence that LCZ696 treatment and TLR2 knockdown attenuated doxorubicin-induced cardiac cell fibrosis and inflammationin vitro .